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Knockdown of MRPL35 promotes cell apoptosis and inhibits cell proliferation in non-small-cell lung cancer

ABSTRACT: Knockdown of MRPL35 promotes cell apoptosis and inhibits cell proliferation in non-small-cell lung cancer

PROVIDER: PRJNA938106 | ENA |

REPOSITORIES: ENA

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Knockdown of MRPL35 promotes cell apoptosis and inhibits cell proliferation in non-small-cell lung cancer

Project description:Background: Non-small cell lung cancer (NSCLC) is a major pathological type of lung cancer. However, its pathogenesis remains largely unclear. MRPL35 is a regulatory subunit of the mitoribosome, which can regulate the assembly of cytochrome c oxidases and play an important role in the occurrence of NSCLC. Methods:The expression of MRPL35 in NSCLC was detected by tissue microarray and immunohistochemistry. H1299 cells were infected with lentivirus to knockdown MRPL35, and the cells were subjected to crystal violet staining to assess the results of colony formation assays. A549 cells were infected by lentiviral particles-expressing shMRPL35 or shControl, and then subcutaneously injected into nude mice. Tumorigenesis in mice was detected by in vivo imaging. The potential pathway of MRPL35 in NSCLC was assessed by Western blotting. Results:MRPL35 was over-expressed in NSCLC tissue compared to para-cancerous and normal tissues. Knockdown of MRPL35 suppressed cell proliferation and decreased NSCLC progression both in vitro and in vivo. The possible molecular mechanisms were also clarified, which indicated that MRPL35 could be involved in cell apoptosis and proliferation by modulating the expression levels of CDK1, BIRC5, CHEK1, STMN1 and MCM2. Knockdown of MRPL35 activated p53 signaling pathway and inhibited cell cycle regulation. Conclusions:The oncogenic role of MRPL35 in NSCLC was potentially mediated through the cell cycle regulatory genes such as BIRC5, STMN1, CDK1, CHEK1 and MCM2, as well as activation of P53 signaling pathway.

2023-05-03 | GSE225959 | GEO

HEXIM knockdown triggers apoptosis-induced proliferation and deregulates Hedgehog signaling

Project description:We address the function of HEXIM, an inhibitor of the general transcriptional elongation regulator P-TEFb which regulates the transcriptional status of many developmental genes, during Drosophila development. We showed that HEXIM knockdown mutants display organs development failure. In the wing disc, it induces apoptosis and affects Hh signaling. The continuous death of proliferative cells is compensated by apoptosis-induced cell proliferation, in a manner similar to that of differentiated cells, together with high levels of Hh and Ci. We completed this analysis with microarrays to characterize the molecular phenotype of HEXIM knockdown during eye differentiation. HEXIM knockdown during eye differentiation was carried out with a UAS-Hexim-RNAi strain crossed with a GMR-Gal4 driver strain (Bloomington stock center)). Adult GMR>RNAi Hexim flies display slightly smaller, rough and often necrosed eyes. Total RNA were collected from isolated heads. We then used microarray to compare the transcriptome of HEXIM knockdown mutant with that of wild type flies.

2014-07-31 | E-GEOD-54590 | biostudies-arrayexpress

HEXIM knockdown triggers apoptosis-induced proliferation and deregulates Hedgehog signaling

2014-07-31 | GSE54590 | GEO

BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer

Project description:BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer

| PRJNA631661 | ENA

Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis Through the Mitochondria‑Dependent Apoptosis in Human Gastric Cancer Cells

Project description:Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis Through the Mitochondria‑Dependent Apoptosis in Human Gastric Cancer Cells

| PRJNA842914 | ENA

TMPRSS4 promotes cell proliferation and inhibits apoptosis in pancreatic ductal adenocarcinoma by activating ERK1/2 signaling pathway

Project description:TMPRSS4 promotes cell proliferation and inhibits apoptosis in pancreatic ductal adenocarcinoma by activating ERK1/2 signaling pathway

| PRJNA714592 | ENA

TMPRSS4 promotes cell proliferation and inhibits apoptosis in pancreatic ductal adenocarcinoma by activating ERK1/2 signaling pathway

Project description:Transmembrane protease serine 4 (TMPRSS4) is upregulated in various kinds of human cancers, including pancreatic cancer. However, its biological function in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In the current study, real-time qPCR, immunohistochemical staining, Western blotting, and database (Cancer Genome Atlas and Gene Expression) analysis revealed remarkable overexpression of TMPRSS4 in PDAC tissue as compared to non-tumor tissue. The TMPRSS4 overexpression was associated with poor prognosis of PDAC patients. Moreover, multivariate analysis revealed that TMPRSS4 serves as an independent risk factor in PDAC. We performed gain-and loss-of-function analysis and found that TMPRSS4 promotes cellular proliferation and inhibits apoptosis of PDAC cells both in vitro and in vivo. Furthermore, we showed that TMPRSS4 might promote cell proliferation and inhibit apoptosis through activating ERK1/2 signaling pathway in pancreatic cancer cells. These findings were validated by using ERK1/2 phosphorylation inhibitor SCH772984 both in vitro and in vivo. Taken together, this study suggests that TMPRSS4 is a proto-oncogene, which promotes initiation and progression of PDAC by controlling cell proliferation and apoptosis. Our findings indicate that TMPRSS4 could be a promising prognostic biomarker and a therapeutic target for the treatment of pancreatic cancer.

2024-03-07 | GSE168918 | GEO

Knockdown PTPRN expression inhibits U87 cell line growth

Project description:Knockdown PTPRN expression inhibits U87 cell line growth

| PRJNA600821 | ENA

Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

Project description:Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

| PRJNA281224 | ENA

CDCA2 inhibits apoptosis and promotes cell proliferation in prostate cancer and is directly regulated by HIF-1α pathway

Project description:CDCA2 inhibits apoptosis and promotes cell proliferation in prostate cancer and is directly regulated by HIF-1α pathway

| PRJNA625006 | ENA