Preliminary study on the cellular and molecular mechanisms of Cms1 ribosomal small subunit homolog promoting hepatocellular carcinoma progression via activation of the homolog family member A/yes-associated protein 1 signaling pathway.

Abstract

Objective: The precise mechanism of action of cms1 ribosomal small subunit homolog (CMSS1) in hepatocellular carcinoma (HCC) is yet unknown, although it may be essential to the malignant evolution of disease. The aim of this study was to reveal the role of CMSS1 in HCC and its possible mechanism.

Material and methods: The expression of CMSS1 in different HCC cell lines was detected by quantitative real-time polymerase chain reaction and Western blot. The expression of CMSS1 in HCC cells was subsequently silenced, and the proliferation capacity of HCC cells was measured by colony formation assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry, and the migration and metastasis capacity of the HCC cells was measured by Transwell assay and Western blot. Finally, ras homolog family member A (RhoA) and yes-associated protein 1 (YAP1) were silenced, and the relationship between CMSS1, RhoA, and YAP1 was further discussed by immunofluorescence, colony formation assay, and EdU assay.

Results: The experimental results showed that CMSS1 is highly expressed in HCC tissues and cell lines (P < 0.001). Further experiments demonstrated that CMSS1 promotes the malignant progression of HCC by activating the RhoA GTPase/YAP1 signaling pathway (P < 0.001). Inhibition of YAP1 could reverse the enhanced proliferation and colony formation ability induced by CMSS1 (P < 0.001). Silencing CMSS1 expression can inhibit epithelial- mesenchymal transition (P < 0.01). Moreover, silencing RhoA reduces the YAP1 nuclear translocation (P < 0.001).

Conclusion: CMSS1 promotes the malignant progression of HCC by activating the RhoA GTPase/YAP1 signaling pathway.