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The authors identified a novel long non-coding RNA (lncRNA), DLGAP1-AS1, that exhibits oncogenic. properties in non-small-cell lung cancer (NSCLC). DLGAP1-AS1 was highly expressed in NSCLC. tissues and cells. Inhibition of lncRNA DLGAP1-AS1 suppressed NSCLC progression both in vitro and. in vivo via the miR-193a-5p/denticleless protein homolog (DTL) axis. This novel regulatory network. provides a potential therapeutic strategy for NSCLC.
Ubiquitin-specific protease 3 (USP3), a cysteine protease, is deubiquitinating enzyme. USP3 is aberrantly expressed in several types of tumors. The authors show that USP3 is an important positive regulator in gallbladder cancer progression, and that pyruvate kinase L/R plays a key role in the progression of GBC.
The authors present a workflow that allows the simultaneous measurement of the whole exome and the transcriptome by next-generation sequencing from formalin-fixed paraffin-embedded tissue sections that were analyzed by matrix-assisted laser desorption ionization mass spectrometry imaging. The data and analyses demonstrate the feasibility and reproducibility of this approach, which expands the possibilities of multi-omics integration in cancer research.
For precancerous/endometrial cancer patients with fertility maintain desire, progestin resistance is the main obstacle of conservative therapy. The authors found that brusatol, as a natural compound, suppresses progestin metabolism through regulating the NRF2-TET1-AKR1C1 pathway to sensitize precancerous/endometrial cancers to progestin and relieve progestin resistance. This study indicates that progestin combined with brusatol may enhance the treatment effects and that AKR1C1 expression patterns may serve as an important biomarker of progestin resistance in endometrial cancer.
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and is associated with limited treatment options. This study elucidates the role of KLHL17 in the development and progression of NSCLC using clinical samples and NSCLC cell lines. The results show that upregulated KLHL17 in NSCLC promotes the proliferation and migration of tumor by activating Ras/MAPK signaling pathway, and suggest that KLHL17 may be a novel therapeutic target for the treatment of NSCLC.
The authors describe a regulatory mechanism for ferroptosis sensitivity that is dependent on circST6GALNAC6 expression levels in bladder cancer. CircST6GALNAC6 inhibits HSPB1 and promotes cell ferroptosis by blocking the phosphorylation site (Ser-15) of HSBP1 and activating the P38 MAPK signaling pathway. Enhancing the expression of circST6GALNAC6 to promote ferroptosis, or using circST6GALNAC6 as a biomarker of ferroptosis sensitivity, is significant for the development and application of ferroptosis intervention methods.
Hyperglycemia induces endoplasmic reticulum stress and increases expression of MAPK10, and 4-phenylbutyric treatment and the knockdown of MAPK10 both alleviate hyperglycaemia-induced myocardial dysfunction, respectively. Therefore, the present study sheds new light on the novel role of MAPK10 in hyperglycemia-induced myocardial dysfunction in db/db mice.
This study shows the potential application of c-Jun phosphorylation upon cisplatin treatment as a biomarker for cisplatin sensitivity in combination with patient-derived tumor organoids (PDOs). We also compared the responses of 6 PDOs to cisplatin with the therapeutic effect of neoadjuvant chemotherapy in 6 matched patients with esophageal squamous cell carcinoma.
GPM6A expression is markedly suppressed in hepatocellular carcinoma and suppresses proliferation and migration of hepatoma cells. Moreover, its low expression is most likely attributed to upregulated miRNA-96-5p but not gene mutation or changes in methylation. These findings indicate that GPM6A may function as an inhibitory gene in chronic information, fibrosis and oncogenic transformation.
This study presents a novel perspective on the influences of the microbiome-cancer axis during tumor development and treatment, in a syngeneic, immunocompetent mammary tumor mouse model. The findings define substantial remodeling of the gut microbiome and changes in the intestinal immune network in response to the orally administered therapeutic Hedgehog inhibitor, Vismodegib, and highlight the dynamic shifts in the abundance of pro- and anti-inflammatory gut microbes during tumor progression and in response to Hedgehog blockade.
The authors identified tissue inhibitor of metalloproteinase-1 (TIMP1) as an important regulator of tissue stiffness in isocitrate dehydrogenase (IDH)-wild type (WT) gliomas. TIMP1 knockdown decreases tissue stiffness, inhibited the expression of tenascin C and fibronectin, and suppressed tumor progression. These results suggest that TIMP1 could be a potential therapeutic target for IDH-WT gliomas.
The levels of m6A and WTAP are elevated in the CD4+ T cells of tolerant kidney transplant recipients. In naïve CD4+ T cells from kidney transplant recipients with immune rejection, WTAP is highly expressed and facilitates Foxo1 transcription by enhancing m6A modification of Foxo1 mRNA in the CDS region, which enhances Foxo1-mediated Foxp3 transcription and subsequent Treg cell differentiation and function.
Idelalisib, a specific inhibitor of phosphoinositide 3-kinase (PI3K) δ, inhibits Akt activation, fibronectin expression and collagen gel contraction induced by transforming growth factor (TGF)-β2 in human RPE cells as well as in an animal model of proliferative vitroretinopathy. These results suggest that idelalisib may be useful for preventing proliferative vitroretinopathy in humans.
The present study elucidates the novel role of PIK3CD in glioblastoma (GBM) progression. Using in vitro and in vivo models of GBM, the authors show that GBM migration, invasion, proliferation and growth affect greatly when the activity of PIK3CD is disrupted by CRISPR/Cas9. Mechanistically, PIK3CD regulates the activity of p21 activated kinase (PPAK3) and plecstrin 2 (PLEK2) through axonogenesis pathway. The findings provide a novel mechanism of PIK3CD-mediated GBM development and suggest PIK3CD might be a target of GBM.
The authors show that CC chemokine receptor 2 (CCR2) overexpression is an independent prognostic marker for diffuse large B-cell lymphoma (DLBCL) and predicts overall survival and progression-free survival in these patients. Blockade of CCR2 signaling with a CCR2 antagonist inhibits tumor cell proliferation, migration, and apoptosis inhibition by activating the PI3K/Akt signaling pathway and inhibiting the p38 MAPK signaling pathway. Furthermore, administration of a CCR2 antagonist decreases tumor growth and dissemination of DLBCL cells and increases survival time in a xenograft model.
Levels of E3 ligase FBXW7 are depressed in radioresistant cells. Overexpression of FBXW7 represses proliferation and colony formation and increases γ-H2AX-positive foci in cultured cells. Overexpression of FBXW7 increases ubiquitination levels and reduces the stability of SOX9, which binds to the CDKN1A promoter to inhibit expression. The authors conclude that FBXW7 inhibits tumorigenesis and apoptosis and enhances radiosensitivity of NSCLC cells via SOX9/CDKN1A.
Lymph node metastasis (LNM) worsens the prognosis of nasopharyngeal cancer (NPC) patients. Thus, bioinformatic analysis was used to determine a key gene, the tyrosine-kinase receptor KITLG, that might play a critical rols in the LNM of NPC. The suppression of KITLG inhibits the proliferation, invasion, and metastasis of NPC cells via the JAK/STAT signaling pathway.
Lung squamous cell carcinoma (LSCC) is a common subtype of lung cancer with high malignancy. The authors show that the kinase PAK2 binds to the transcription factor SOX2 and activates the oncogene DEK, thus contributing to the malignant behavior of LSCC cells. This work provides new therapeutic targets and insightful information for enhancing targeted therapy of LSCC.
The authors developed a concise and efficient survival analysis model, named CNN-Cox. The survival prediction performance of this model on RNA-seq datasets of various cancers from The Cancer Genome Atlas cohort was discussed and compared with other state-of-the-art survival analysis methods. They also conducted protein–protein interaction network analysis to identify potential prognostic genes and analyzed the biological function of 13 hub genes for a lung adenocarcinoma dataset.