ArticleCancer gene therapy2022
Silencing of RND3/RHOE inhibits the growth of human hepatocellular carcinoma and is associated with reversible senescence.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- TMEM121 suppresses cervical cancer cell proliferation and migration via interaction with the ERK pathway.American journal of cancer research · 2026Article
- Racial disparities in hepatocellular carcinoma: a TCGA-based gene expression study of Caucasian and Asian populations.Exploration of targeted anti-tumor therapy · 2025Article
- Mechanistic insights into SIRT7 and EZH2 regulation of cisplatin resistance in bladder cancer cells.Cell death & disease · 2024Article
- Mechanisms and significance of entosis for tumour growth and progression.Cell death discovery · 2024Review
- Loss of RND3/RHOE controls entosis through LAMP1 expression in hepatocellular carcinoma.Cell death & disease · 2024Article
- Identification of the hub genes associated with prostate cancer tumorigenesis.Frontiers in oncology · 2023Article
- RHO GTPase family in hepatocellular carcinoma.Experimental hematology & oncology · 2022Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rnd3/RhoE is an atypical Rho GTPase family member, known to be deregulated in many types of cancer. Previously, we showed that RND3 expression is downregulated in hepatocellular carcinoma (HCC) cell lines and tissues. In cancer cells, Rnd3 is involved in the regulation of cell proliferation and cell invasion. The implication of Rnd3 in HCC invasion was importantly studied whereas its role in cell growth needs further investigation. Thus, in this work, we aimed to better understand the impact of Rnd3 on tumor hepatocyte proliferation. Our results indicate that the silencing of RND3 induces a cell growth arrest both in vitro in 2D and 3D culture conditions and in vivo in tumor xenografts. The growth alteration after RND3 silencing in HCC cells is not due to an increase of cell death but to the induction of senescence. This RND3 knockdown-mediated phenomenon is dependent on the decrease of hTERT expression. Interestingly, after re-expression of RND3, these cells are able to bypass senescence and regain the ability to proliferate, with a re-expression of hTERT. Given that a low expression of Rnd3 is linked to the presence of satellite nodules in HCC, the transient senescence state observed might play a role in cancer progression.
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