ArticleCellular & molecular biology letters2019
siRNA against TSG101 reduces proliferation and induces G0/G1 arrest in renal cell carcinoma - involvement of c-myc, cyclin E1, and CDK2.
Article in Cellular & molecular biology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Antitumor Activity ofMarine drugs · 2025Article
- Overexpression of TSG101 causes the development of adenosquamous mammary carcinoma.Breast cancer research : BCR · 2025Article
- Candidate biomarkers for treatment benefit from sunitinib in patients with advanced renal cell carcinoma using mass spectrometry-based (phospho)proteomics.Clinical proteomics · 2023Article
- PPP1R14D promotes the proliferation, migration and invasion of lung adenocarcinoma via the PKCα/BRAF/MEK/ERK signaling pathway.International journal of oncology · 2022Article
- tRF-3013b inhibits gallbladder cancer proliferation by targeting TPRG1L.Cellular & molecular biology letters · 2022Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway in HeLa cells.Bioengineered · 2022Article
- Knockdown of ANXA10 inhibits proliferation and promotes apoptosis of papillary thyroid carcinoma cells by down-regulating TSG101 thereby inactivating the MAPK/ERK signaling pathway.Journal of bioenergetics and biomembranes · 2021Article
- High expression of tumor susceptibility gene 101 (TSG101) is associated with more aggressive behavior in colorectal carcinoma.Journal of cancer research and clinical oncology · 2021Article
- MiR-17-5p-mediated endoplasmic reticulum stress promotes acute myocardial ischemia injury through targeting Tsg101.Cell stress & chaperones · 2021Article
- The Multifaceted Roles of the Tumor Susceptibility Gene 101 (TSG101) in Normal Development and Disease.Cancers · 2020Review
- LncRNA PCGEM1 promotes renal carcinoma progression by targeting miR-433-3p to regulate FGF2 expression.Cancer biomarkers : section A of Disease markers · 2020Article
- TCF 4 tumor suppressor: a molecular target in the prognosis of sporadic colorectal cancer in humans.Cellular & molecular biology letters · 2020Article
- Editorial focus: understanding off-target effects as the key to successful RNAi therapy.Cellular & molecular biology letters · 2019Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe tumor susceptibility gene 101 (TSG101) is closely associated with various tumor types, but its role in the pathogenesis of renal cell carcinoma (RCC) is still unknown. This study used RNA interference to silence the expression of TSG101 in RCC cell lines and explore the role of TSG101 in RCC.
methodsImmunohistochemistry and western blot were performed to detect the expression of TSG101 in 15 paired renal tumor samples. A small interfering RNA (siRNA) targeting TSG101 was transfected into A498 and 786-O cell lines. The Cell Counting Kit-8 (CCK-8) assay and colony formation assay were used to observe the changes in cell proliferation after transfection. Flow cytometry was used to detect the effect on the cell cycle. Western blot was conducted to study the changes of related functional proteins.
resultsThe expression of TSG101 was higher in RCC tissues than in adjacent normal tissues. The CCK-8 assay showed that the proliferation and colony formation of the A498 and 786-O cell lines were attenuated after suppression of TSG101. Flow cytometry showed that silencing of TSG101 induced G0/G1 arrest. The western blot results revealed that the levels of cell cycle-related proteins (c-myc, cyclin E1 and cyclin-dependent kinase 2 (CDK2)) were markedly decreased in the siRNA groups.
conclusionsTSG101 promotes proliferation of RCC cells. This positive effect on tumor growth involves activation of c-myc and cyclin E1/CDK2 and their effect on cell cycle distribution.
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