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Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment

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A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Methods and Technologies Development".

Deadline for manuscript submissions: 29 January 2025 | Viewed by 13647

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Special Issue Editor

Dr. Anthony Taylor

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Guest Editor

Leicester Medical School, University of Leicester, Leicester, UK
Interests: gynecological cancer; ovarian disorders; endocannabinoid system; molecular mechanism

Special Issue Information

Dear Colleagues,

It is clear that the incidence of gynaecological cancers is on the increase and due to the different forms of gynaecological cancer (ovarian, oviductal, endometrial, cervical and vulval), different therapeutic approaches are required. Additionally, the efficacy of various targeted therapies in different cancer subtypes suggests that treatment choices in the near future will be dependent on technology. Data from preclinical, clinical, and observational studies have revealed many new technologies such as robotic surgery (for endometrial cancer), iKnife and MS/MS molecular modelling (for ovarian cancer) and Zedscan (electrical impedance) measurement for cervical cancer. Associated methodologies have also improved patient outcomes and survival, with this trend likely to continue.

This open-access Special Issue will bring together original research and review articles on molecular oncology and the use of emerging technologies in relation to the early detection and treatment of cancers. It highlights new findings, methods, and technical advances in gynaecological cancer research. The main feature of this Special Issue is to provide open-source sharing of significant works in the field of gynaecological cancer that will increase our understanding of cancer development, and may lead to the discovery of new molecular diagnostic technologies and better targeted therapeutics.

Topics include but are not limited to:

Molecular methods for better gynaecological cancer screening and detection.
New technology for better targeted therapies to prevent cancer development and metastases.
Identification and new aspects of cellular signalling molecules and pathways for target discovery, patient prognosis, future drug design, and better patient outcomes.

Dr. Anthony Taylor
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

gynaecological cancer
robotic surgery
cancer screening and detection
cellular signalling molecules
pathways cellular signalling

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Published Papers (7 papers)

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Research

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11 pages, 1246 KiB

Open AccessArticle

Effects of PARP Inhibitors on Subsequent Platinum-Based Chemotherapy in Patients with Recurrent Ovarian Cancer

by Tetsuya Kokabu, Yosuke Tarumi, Kota Aoki, Ayaka Okamura, Kohei Aoyama, Hisashi Kataoka, Kaori Yoriki and Taisuke Mori

Cancers 2024, 16(15), 2651; https://doi.org/10.3390/cancers16152651 - 25 Jul 2024

Viewed by 637

Abstract

The clinical outcomes in patients with ovarian cancer have been significantly improved by Poly(adenosine diphosphate–ribose) polymerase inhibitors (PARP-is). However, the best therapeutic strategy for recurrence during PARP-i maintenance therapy remains unknown. Herein, we elucidated the efficacy of platinum-based chemotherapy after PARP-i treatment in recurrent ovarian cancer. Eligible patients had experienced relapses during PARP-i maintenance therapy lasting at least 6 months and had received subsequent platinum-based chemotherapy at our institution between January 2019 and March 2024. Progression-free survival (PFS), overall survival (OS), and risk factors for PFS were evaluated. Sixty-six patients were assessed for eligibility and eighteen were enrolled. The median follow-up period was 14.5 months. The PFS and OS of all patients were 6.5 and 17.6 months, respectively. The evaluation of the risk factors for PFS revealed that age, pathological type, duration of PARP-i maintenance therapy, prior lines of chemotherapy, and PARP-i dose reduction were not significant prognostic markers. However, bevacizumab use in subsequent therapies significantly extended the PFS. The median PFS was 3.1 months in the chemotherapy-alone group and 8.9 months in the chemotherapy with bevacizumab group (log-rank p = 0.022). Platinum-based chemotherapy with bevacizumab in subsequent therapies would provide substantial benefits in the PFS of patients with recurrent ovarian cancer. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

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16 pages, 3697 KiB

Open AccessArticle

Anticancer Effects of BRD4 Inhibitor in Epithelial Ovarian Cancer

by Yeorae Kim, Wook-Ha Park, Dong-Hoon Suh, Kidong Kim, Jae-Hong No and Yong-Beom Kim

Cancers 2024, 16(5), 959; https://doi.org/10.3390/cancers16050959 - 27 Feb 2024

Viewed by 1322

Abstract

Efforts have been made to develop bromodomain inhibitors as cancer treatments. Sub-pathways, particularly in ovarian cancer, affected by bromodomain-containing protein (BRD) remain unclear. This study verified the antitumor effects of a new drug that can overcome OPT-0139-chemoresistance to treat ovarian cancer. A mouse xenograft model of human ovarian cancer cells, SKOV3 and OVCAR3, was used in this study. Cell viability and proliferation were assessed using MTT and ATP assays. Cell cycle arrest and apoptosis were determined using flow cytometry. BRD4 and c-Myc expression and apoptosis-related molecules were detected using RT-PCR and real-time PCR and Western blot. We confirmed the OPT-0139 effect and mechanism of action in epithelial ovarian cancer. OPT-0139 significantly reduced cell viability and proliferation and induced apoptosis and cell cycle arrest. In the mouse xenograft model, significant changes in tumor growth, volume, weight, and BRD4-related gene expression were observed, suggesting the antitumor effects of BRD4 inhibitors. Combination therapy with cisplatin promoted apoptosis and suppressed tumor growth in vitro and in vivo. Our results suggest OPT-0139, a BRD4 inhibitor, as a promising anticancer drug for the treatment of ovarian cancer by inhibiting cell proliferation, decreasing cell viability, arresting cell cycle, and inducing apoptosis. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

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15 pages, 5047 KiB

Open AccessArticle

Novel LIPA-Targeted Therapy for Treating Ovarian Cancer

by Alexia B. Collier, Suryavathi Viswanadhapalli, Rahul Gopalam, Tae-Kyung Lee, Kara Kassees, Karla Parra, Gaurav Sharma, Tanner C. Reese, Xihui Liu, Xue Yang, Behnam Ebrahimi, Uday P. Pratap, Megharani Mahajan, William C. Arnold, Adriana Baker, Chia-Yuan Chen, Scott Terry Elmore, Panneerdoss Subbarayalu, Gangadhara R. Sareddy, Philip T. Valente, Edward R. Kost, Jung-Mo Ahn and Ratna K. Vadlamudi Show full author list Hide full author list

Cancers 2024, 16(3), 500; https://doi.org/10.3390/cancers16030500 - 24 Jan 2024

Viewed by 1974

Abstract

Ovarian cancer (OCa) is the most lethal form of gynecologic cancer, and the tumor heterogeneities at the molecular, cellular, and tissue levels fuel tumor resistance to standard therapies and pose a substantial clinical challenge. Here, we tested the hypothesis that the heightened basal endoplasmic reticulum stress (ERS) observed in OCa represents an exploitable vulnerability and may overcome tumor heterogeneity. Our recent studies identified LIPA as a novel target to induce ERS in cancer cells using the small molecule ERX-41. However, the role of LIPA and theutility of ERX-41 to treat OCa remain unknown. Expression analysis using the TNMplot web tool, TCGA data sets, and immunohistochemistry analysis using a tumor tissue array showed that LIPA is highly expressed in OCa tissues, compared to normal tissues. ERX-41 treatment significantly reduced the cell viability and colony formation ability and promoted the apoptosis of OCa cells. Mechanistic studies revealed a robust and consistent induction of ERS markers, including CHOP, elF2α, PERK, and ATF4, upon ERX-41 treatment. In xenograft and PDX studies, ERX-41 treatment resulted in a significant reduction in tumor growth. Collectively, our results suggest that ERX-41 is a novel therapeutic agent that targets the LIPA with a unique mechanism of ERS induction, which could be exploited to treat heterogeneity in OCa. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

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Figure 1

Figure 1
LIPA is overexpressed in OCa. (A) Boxplots of LIPA gene expression in normal (n = 133) and tumor (n = 374) gene array data. Data was obtained from the TNMplot database. (B) Association of LIPA gene expression with the overall survival of OCa patients using KM plotter. (C,D) Samples from 4 subtypes of OCa and normal ovarian tissue were evaluated for LIPA expression using tissue microarray, with representative images (C) and quantitation (D). Scale bar represents 100 µm. Data are represented as mean ± SEM. **** p < 0.0001. Full article ">Figure 2
ERX-41 is potent against OCa cells in vitro. (A,B) Effect of ERX-41 on the cell viability of established (A) and patient-derived primary OCa cells (B) was determined using MTT assay. (C,D) Established and primary OCa cells were treated with the indicated doses of ERX-41, and the colony formation was examined after 14 days (C). The numbers of colonies were quantified and were shown as bar graphs in the lower panel (D). (E,F) The effect of ERX-41 on the cell invasion of OCa cells was determined using BioCoat Matrigel invasion chamber assays. Images are shown in panel (E), scale bar represents 100 µm (E), and the quantitation of the percentage of cells invaded is shown in panel (F). (G) The effects of ERX-41 (500 nmol/L) on the apoptosis of established and patient-derived OCa cells were determined using Annexin V/PI staining. Data are represented as mean ± SEM. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. Full article ">Figure 3
ERX-41 induces ER stress (ERS) in OCa. (A) The time course of the effects of ERX-41 (1 µM) on the mRNA expressions of ERS genes, XBP1s, and CHOP in ES2, SKOV3, OVCAR3, and OVCAR4 cells. (B) RT-PCR analysis shows the time course of the effects of ERX-41 (1 µM) on the expression of XBP1 (unspliced (XBP1u) and spliced (XBP1s)) in ES2, OVCAR3, and OCa39 cells. (C) OCa cells were treated with ERX-41 (1 µM, 6 h), and the statuses of ERS genes were measured by RT-qPCR. (D) OCa cells were treated with ERX-41 for indicated time points, and the statuses of the activations of UPR components were analyzed by Western blotting. (E) Transmission electron microscopy of OVCAR8 cells shows the effects of vehicle and ERX-41 treatments on subcellular structures at 8 h; ER is outlined with yellow arrowheads. Scale bar represents 400 nm. Data are represented as mean ± SEM. ** p < 0.01; *** p < 0.001; **** p < 0.0001. Full article ">Figure 4
LIPA is the target of ERX-41. (A) LIPA-KO in SKOV3 cells was confirmed using Western blotting. (B) The effect of the KO of LIPA in SKOV3 cells on the dose–response curve to ERX-41 was determined using CellTiter-Glo assays. (C) Dose–response curves to increasing concentrations of ERX-41 in KO, KO + WT, and KO + MT SKOV3 cells were performed by the CellTiter-Glo assay. (D) The effect of LIPA-KO on the activity of ERX-41 in reducing the colony formation was determined. (E) Quantitation of colonies are shown. (F) SKOV3-WT and LIPA-KO cells were treated with ERX-41 for indicated time points, and the status of the splicing of XBP1 was measured by RT-PCR. Data are represented as mean ± SEM. **** p < 0.0001; ns, not significant. Full article ">Figure 5
ERX-41 effectively reduces the growth of patient-derived organoids (PDOs). (A,B) Using 3D CellTtiter-Glo assays, the impact of ERX-41 treatment on the viability of PDOs was evaluated (A). Representative pictures of PDOs cultured with or without ERX-41 treatment are shown (B). Data are represented as mean ± SEM. * p < 0.05; *** p < 0.001; **** p < 0.0001. Full article ">Figure 6
ERX-41 treatment suppresses OCa xenograft tumor growth in vivo. (A–C) SKOV3 cells were injected subcutaneously into SCID mice. Following tumor establishment, mice were randomly assigned to receive either vehicle (control) or ERX-41 (10 mg/kg body weight) five days a week through i.p. injection. Tumor volume was assessed at 3–5-day intervals (A). Tumor weights (B) and tumor pictures (C) are shown. (D–F) Following the establishment of subcutaneous OVCAR8 xenograft tumors, SCID mice were randomly assigned to receive either vehicle (control) or ERX-41 (10 mg/kg body weight) five days a week through i.p. injection. Tumor volume was assessed at 3–5-day intervals (D). Tumor weights (E) and tumor pictures (F) are shown. (G) SKOV3 and OVCAR8 xenograft tumor samples from the vehicle (control) and ERX-41 treatment groups were processed by IHC for Ki67 (proliferation marker) and quantitated (H). Scale bar represents 100 µm. Data are represented as mean ± SEM. * p < 0.05; ** p < 0.01; **** p < 0.0001. Full article ">

22 pages, 4318 KiB

Open AccessArticle

Identification of Potentially Novel Molecular Targets of Endometrial Cancer Using a Non-Biased Proteomic Approach

by Anthony H. Taylor, Justin C. Konje and Thangesweran Ayakannu

Cancers 2023, 15(18), 4665; https://doi.org/10.3390/cancers15184665 - 21 Sep 2023

Cited by 1 | Viewed by 1510

Abstract

The present study was aimed at identifying novel proteins in endometrial cancer (EC), employing proteomic analysis of tissues obtained after surgery. A differential MS-based proteomic analysis was conducted from whole tissues dissected from biopsies from post-menopausal women, histologically confirmed as endometrial cancer (two endometrioid and two serous; n = 4) or normal atrophic endometrium (n = 4), providing 888 differentially expressed proteins with 246 of these previously documented elsewhere as expressed in EC and 372 proteins not previously demonstrated to be expressed in EC but associated with other types of cancer. Additionally, 33 proteins not recorded previously in PubMed as being expressed in any forms of cancer were also identified, with only 26 of these proteins having a publication associated with their expression patterns or putative functions. The putative functions of the 26 proteins (GRN, APP, HEXA, CST3, CAD, QARS, SIAE, WARS, MYH8, CLTB, GOLIM4, SCARB2, BOD1L1, C14orf142, C9orf142, CCDC13, CNPY4, FAM169A, HN1L, PIGT, PLCL1, PMFBP1, SARS2, SCPEP1, SLC25A24 and ZC3H4) in other tissues point towards and provide a basis for further investigation of these previously unrecognised novel EC proteins. The developmental biology, disease, extracellular matrix, homeostatic, immune, metabolic (both RNA and protein), programmed cell death, signal transduction, molecular transport, transcriptional networks and as yet uncharacterised pathways indicate that these proteins are potentially involved in endometrial carcinogenesis and thus may be important in EC diagnosis, prognostication and treatment and thus are worthy of further investigation. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

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Figure 1
Scaffold Proteome analyses for correct spectral identification. The upper panel shows the number of peptide spectra assigned correctly (pink bars) compared to number of peptide spectra assigned incorrectly (green bars) together with their relative distributions (red and blue lines). The lower panel shows the log-transformed data for the number of spectra plotted against the negative log of the expected value of spectra based on the discriminant score shown in Panel A. Only 1 spectral line is a higher level than expected and that associates with serum albumin in both the control and cancer samples. The software can be accessed from <a href="http://www.proteomesoftware.com" target="_blank">www.proteomesoftware.com</a>, last accessed 6 September 2023. Full article ">Figure 2
Scatterplot for the relative quantities of proteins identified in 4 control (atrophic) and 4 endometrial cancer (cancer) samples. The upper panel (A) shows the raw data, whilst the middle panel (B) shows the log-transformed data once the proteins outside the 3 standard deviations had been omitted. The protein highlighted with a yellow circle is serum albumin and was the most abundant protein in the atrophic samples (the data point for the cancer sample is outside the 3 standard deviations range). The spread of data is consistent with a high probability of protein identification. The lower panel (C) shows a histogram of positive peptide sequences identified in the biological samples. The data indicate the number of positive peptide sequences identified in the individual biological samples (control/atrophic: pink bars) and (endometrial cancer/cancer: blue bars) for the protein with the most abundant peptide spectra—serum albumin (highlighted in panel A). Full article ">Figure 3
Venn diagram and bar charts for proteins identified using X! Tandem and Mascot. Venn diagrams (A) are used to show that a total of 1851 proteins were originally identified, of which 888 were common to both control (atrophic) and endometrial cancer (cancer) samples. Only 300 proteins were found solely in the control tissues, and 663 were only found in the cancer tissues. After close examination of the peptide identities, 4 proteins were duplicated in the cancer tissues and so were eliminated from further analyses (second Venn diagram). Gene ontology (GO) pathway analysis of the 663 proteins found only in endometrial cancer matched the genes identified to 21 biological processes (B) and to 8 molecular functions (C). The % of genes in each category is indicated. Full article ">Figure 4
Functional analysis of cancer-specific protein pathways and interactions. The diagram depicts functional densities for the proteins identified as being exclusive to endometrial cancer. The data output is direct from the Reactome application. Note the enrichment of proteins in signal transduction, cell cycle, programmed cell death, metabolism, disease processes and reproduction. Also note that two distinct networks are prevalent: one on the left-hand side of the figure and focused on signal transduction and another on the right-hand side focused on the cell cycle. Full article ">Figure 5
Expression of proteins unique to endometrial cancer. Panel (A) shows an expression heatmap for the 26 proteins identified to be uniquely expressed in EC. The fold-expression is related to the mean number of peptide spectra of the atrophic samples. When no peptide signal was identified in the atrophic samples, the expression in the serous samples was relative to the mean of all peptide spectra in the 4 atrophic controls. Panel (B) shows a list of proteins found only in the endometrioid (Type 1 EC) samples, serous (Type 2 EC) samples or both types of EC. Full article ">

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12 pages, 585 KiB

Open AccessReview

Serum Proteomic Signatures in Cervical Cancer: Current Status and Future Directions

by Chaston Weaver, Alisha Nam, Caitlin Settle, Madelyn Overton, Maya Giddens, Katherine P. Richardson, Rachael Piver, David P. Mysona, Bunja Rungruang, Sharad Ghamande, Richard McIndoe and Sharad Purohit

Cancers 2024, 16(9), 1629; https://doi.org/10.3390/cancers16091629 - 24 Apr 2024

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Abstract

In 2020, the World Health Organization (WHO) reported 604,000 new diagnoses of cervical cancer (CC) worldwide, and over 300,000 CC-related fatalities. The vast majority of CC cases are caused by persistent human papillomavirus (HPV) infections. HPV-related CC incidence and mortality rates have declined worldwide because of increased HPV vaccination and CC screening with the Papanicolaou test (PAP test). Despite these significant improvements, developing countries face difficulty implementing these programs, while developed nations are challenged with identifying HPV-independent cases. Molecular and proteomic information obtained from blood or tumor samples have a strong potential to provide information on malignancy progression and response to therapy in CC. There is a large amount of published biomarker data related to CC available but the extensive validation required by the FDA approval for clinical use is lacking. The ability of researchers to use the big data obtained from clinical studies and to draw meaningful relationships from these data are two obstacles that must be overcome for implementation into clinical practice. We report on identified multimarker panels of serum proteomic studies in CC for the past 5 years, the potential for modern computational biology efforts, and the utilization of nationwide biobanks to bridge the gap between multivariate protein signature development and the prediction of clinically relevant CC patient outcomes. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

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10 pages, 258 KiB

Open AccessReview

HER2 Oncogene as Molecular Target in Uterine Serous Carcinoma and Uterine Carcinosarcoma

by Blair McNamara, Levent Mutlu, Michelle Greenman, Justin Harold and Alessandro Santin

Cancers 2023, 15(16), 4085; https://doi.org/10.3390/cancers15164085 - 14 Aug 2023

Viewed by 2143

Abstract

Uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS) are two rare histologic variants of uterine carcinoma, with distinct molecular profiles and aggressive metastatic potential. As the effectivity of traditional platinum-based chemotherapy for USC and UCS is low, and there are high rates of resistance and recurrence, the development of novel targeted therapeutics is needed. Human epidermal growth factor receptor 2 (HER2) has proven to be an oncogene of increasing interest in these cancers, as HER2 protein overexpression and/or c-ERBB2 gene amplification ranges from ~30 to 35% in USC, and between ~15 and 20% in UCS. This review summarizes the existing clinical and preclinical evidence, as well as ongoing clinical trials of HER2-targeting therapeutics, and identifies potential areas of further development and inquiry. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

18 pages, 1594 KiB

Open AccessReview

An Overview of Ovarian Cancer: The Role of Cancer Stem Cells in Chemoresistance and a Precision Medicine Approach Targeting the Wnt Pathway with the Antagonist sFRP4

by Lavanya Varier, S. Mohana Sundaram, Naisarg Gamit and Sudha Warrier

Cancers 2023, 15(4), 1275; https://doi.org/10.3390/cancers15041275 - 17 Feb 2023

Cited by 9 | Viewed by 3837

Abstract

Ovarian cancer is one of the most prevalent gynecological cancers, having a relatively high fatality rate with a low five-year chance of survival when detected in late stages. The early detection, treatment and prevention of metastasis is pertinent and a pressing research priority as many patients are diagnosed only in stage three of ovarian cancer. Despite surgical interventions, targeted immunotherapy and adjuvant chemotherapy, relapses are significantly higher than other cancers, suggesting the dire need to identify the root cause of metastasis and relapse and present more precise therapeutic options. In this review, we first describe types of ovarian cancers, the existing markers and treatment modalities. As ovarian cancer is driven and sustained by an elusive and highly chemoresistant population of cancer stem cells (CSCs), their role and the associated signature markers are exhaustively discussed. Non-invasive diagnostic markers, which can be identified early in the disease using circulating tumor cells (CTCs), are also described. The mechanism of the self-renewal, chemoresistance and metastasis of ovarian CSCs is regulated by the Wnt signaling pathway. Thus, its role in ovarian cancer in promoting stemness and metastasis is delineated. Based on our findings, we propose a novel strategy of Wnt inhibition using a well-known Wnt antagonist, secreted frizzled related protein 4 (sFRP4), wherein short micropeptides derived from the whole protein can be used as powerful inhibitors. The latest approaches to early diagnosis and novel treatment strategies emphasized in this review will help design precision medicine approaches for an effective capture and destruction of highly aggressive ovarian cancer. Full article

(This article belongs to the Special Issue Gynecological Cancer: Molecular Oncology and the Use of Emerging Technologies in Relation to Early Detection and Treatment)

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Figure 1
Summary of the widely used treatment strategies for ovarian cancer based on surgical staging and other treatment options in the case of disease recurrence. Full article ">Figure 2
Wnt signaling pathways. Wnt canonical (β-catenin dependent) and Wnt non-canonical (Planar cell polarity and Calcium) pathways. AP-1, Activation protein 1; APC, Adenomatosis polyposis coli; Ca2+, Calcium; CalN, Calcineurin; CAMKII, Calcium-calmodulin-dependent kinase II; Cdc42, Cell division control protein 42 homolog; CK1α, Casein kinase 1 alpha; CREB, cAMP response element-binding protein; DAAM1/2, Disheveled-associated activator of morphogenesis 1/2; DAG, Diacylglycerol; Dkk, Dickkopf; Dvl, Disheveled; FZD, Frizzled; GSK3β, Glycogen synthase kinase 3β; IP3, Inositol 1,4,5-triphosphate; JNK, c-Jun N-terminal kinase; LEF, Lymphoid enhancer-binding factors; LRP 5/6, Low-density lipoprotein receptor-related protein 5 or 6; MAP2K 4/7, Mitogen-activated protein kinase kinase 4/7; MAP3Ks, Mitogen-activated protein kinase kinase kinase; NFAT, Nuclear factor of activated T cells; NFκB, Nuclear factor kappa light chain enhancer of activated B cells; NLK, Nemo-like kinase; PDE, Phosphodiesterase; PKC, Protein kinase C; PKG, Protein kinase G; PLC, Phospholipase C; Rac, Ras-related C3 botulinum toxin substrate; RhoA, Ras homolog family member A; ROCK, Rho Kinase; ROR2, RAR-related orphan receptor 2; Ryk, receptor-like tyrosine kinase; sFRP, Secreted frizzled related protein; TCF, Transcription factors T cell factor; WIF, Wnt inhibitory factor; Wnt, Wingless-type MMTV integration site. Full article ">Figure 3
Differential inhibition of Wnt β-catenin-dependent signaling pathway by sFRP4 and its micropeptides. sFRP4 antagonizes Wnt β-catenin-dependent signaling pathway by (i) binding to FZD via its cysteine-rich domain (CRD) and (ii) binding with Wnt via its netrin-like domain (NLD). SC301 derived from CRD domain binds to FZD, whereas SC401 derived from NLD domain binds with Wnt. Inhibition of Wnt signaling leads to phosphorylation of β-catenin and its subsequent proteasomal degradation. Lack of β-catenin–TCF/LEF interaction in the nucleus causes suppression of angiogenesis and cancer stem cell (CSC) genes along with activation of apoptosis. CRD, Cysteine-rich domain; CSC, Cancer stem cell; NLD, Netrin-like domain. Full article ">

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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: The Emerging Therapeutic Use of Tumor Suppressive MicroRNA-7 in Cervical Cancer
Author: Roy
Highlights: MicroRNA-7 down regulates expression of EGFR and inhibits cell growth and migration in cervical cancer cells. Exosomes can be used to deliver miR-7 to target cancer cells Exosomal miR-7 inhibits cervical cancer proliferation and migration MiRNA-7 has great therapeutic promise in cervical cancer

Title: cervical neuroendocrine small cell carcinoma
Authors: Tze-Chien Chen
Affiliation: Mackay Medical College, Taipei, Taiwan

Title: A Bittersweet Symphony: Galectins, Glycans and High Grade Serous Ovarian Cancer (HGSOC)
Authors: Deirdre Coombe
Affiliation: Curtin Medical School, Pharmacy and Biomedical Sciences, Curtin Health Innovation Research Institute, Faculty of Health Sciences, Curtin University, Perth, WA 6102, Australia

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