The effect of RhoC siRNA on the invasiveness and proliferation of human cervical cancer cell line SiHa cells

He, Xiaoqi; Qian, Ying; Cai, Huilan; Wang, Zehua

doi:10.1007/s11596-008-0611-x

Cited by 6 publications

(4 citation statements)

References 17 publications

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“…In accordance with its contribution to motility and invasion of several cancers (van Golen et al, 2000b;He et al, 2008), our data show that RhoC contributes to tumour progression by affecting invasion, anoikis resistance, tumour growth and angiogenesis in cervical carcinoma cell lines. We show that RhoC drives tumour progression by regulating invasion, metastasis, tumour growth and angiogenesis ( Figure 1).…”

Section: Discussionsupporting

confidence: 89%

“…It has also been shown to regulate tumour progression in various carcinomas (Suwa et al, 1998;Clark et al, 2000;Kleer et al, 2002;Kondo et al, 2004). He et al (2008) showed that RhoC-siRNA (short-interfering RNA) reduced adhesion to Matrigel invasion and migration of SiHa cells. Studies indicate that a cross-talk exists between RhoC and other signalling molecules such as MAPK and vascular endothelial growth factor (Vegf).…”

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confidence: 99%

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Notch1 regulates the functional contribution of RhoC to cervical carcinoma progression

et al. 2009

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Background: The role of Notch signalling in human epithelial cancers is of immense interest. In this study, we examine the interplay between Notch signalling and RhoC, a well-established molecular factor in metastasis. By linking the function of Notch and RhoC, we further strengthen the notion that there is a pro-oncogenic role of Notch signalling in human cervical cancers. Methods: RhoC protein expression in cervical carcinoma cell lines was assessed by western blotting. Using CaSki and SiHa cells (cervical carcinoma cells lines), we show that RhoC contributes to wound healing, invasion and migration, anoikis resistance, colony formation, in vitro tube formation and tumour formation. Immunohistochemical studies were carried out to assess the co-expression of RhoC, pAkt and Notch1 in clinical sections. Results: An assessment of the changes associated with epithelial-to-mesenchymal transition (EMT) shows that both Notch1 and RhoC have similar phenotypic contribution to EMT. Rho activity assessment on Notch1 inhibition with DAPT shows decreased RhoC activity. We further show that constitutively active RhoC rescues the phenotypic effect of Notch1 inactivation, and a comparison of Notch1 with RhoC expression shows an overlap between the two proteins in the same areas of the tissue. Conclusion: This study has provided evidence to suggest that RhoC is an effector of Notch1 in cervical carcinoma.

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Section: Discussionsupporting

confidence: 89%

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confidence: 99%

Notch1 regulates the functional contribution of RhoC to cervical carcinoma progression

et al. 2009

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“…Moreover, it has been shown that expression of some Rho-GTPases and their regulatory proteins is altered in human cancers such as prostate, colon, lung, and breast cancer [18]. Cell culture experiments showed that RhoC regulates invasion and motility of cervical cancer cells [19,20]. Furthermore, it has been reported that RhoC is overexpressed in biopsies from squamous carcinoma of the cervix (SCC) and cervical intraepithelial neoplasia (CIN) II/III when compared to normal cervical epithelium and CIN I [21].…”

Section: Introductionmentioning

confidence: 99%

Nuclear expression of Rac1 in cervical premalignant lesions and cervical cancer cells

et al. 2012

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BackgroundAbnormal expression of Rho-GTPases has been reported in several human cancers. However, the expression of these proteins in cervical cancer has been poorly investigated. In this study we analyzed the expression of the GTPases Rac1, RhoA, Cdc42, and the Rho-GEFs, Tiam1 and beta-Pix, in cervical pre-malignant lesions and cervical cancer cell lines.MethodsProtein expression was analyzed by immunochemistry on 102 cervical paraffin-embedded biopsies: 20 without Squamous Intraepithelial Lesions (SIL), 51 Low- grade SIL, and 31 High-grade SIL; and in cervical cancer cell lines C33A and SiHa, and non-tumorigenic HaCat cells. Nuclear localization of Rac1 in HaCat, C33A and SiHa cells was assessed by cellular fractionation and Western blotting, in the presence or not of a chemical Rac1 inhibitor (NSC23766).ResultsImmunoreacivity for Rac1, RhoA, Tiam1 and beta-Pix was stronger in L-SIL and H-SIL, compared to samples without SIL, and it was significantly associated with the histological diagnosis. Nuclear expression of Rac1 was observed in 52.9% L-SIL and 48.4% H-SIL, but not in samples without SIL. Rac1 was found in the nucleus of C33A and SiHa cells but not in HaCat cells. Chemical inhibition of Rac1 resulted in reduced cell proliferation in HaCat, C33A and SiHa cells.ConclusionRac1 is expressed in the nucleus of epithelial cells in SILs and cervical cancer cell lines, and chemical inhibition of Rac1 reduces cellular proliferation. Further studies are needed to better understand the role of Rho-GTPases in cervical cancer progression.

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“…Previous studies suggested that the RhoC gene was involved in the occurrence and development of liver cancer, and that a close association existed between the high expression of RhoC and the phenotype of hepatocellular carcinoma regarding cell invasion and metastasis (38). Previous studies demonstrated that RhoA/C was highly expressed in a variety of malignancies, participated in the adhesion and migration of tumor cells, and markedly promoted the occurrence and development of tumors (39)(40)(41)(42). As a novel tumor marker, Rho can be applied to distinguish between benign and malignant lesions, and may help to assess the ability of tumor metastasis and prognosis (43).…”

Section: Discussionmentioning

confidence: 99%

Effects of silencing endothelin-1 on invasion and vascular formation in lung cancer

Zhang

Chen

et al. 2017

Oncology Letters

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Abstract. Endothelin-1 (ET-1), which exists not only in the vascular endothelium but is also widely present in various tissues and cells, is an important cardiovascular regulatory factor that serves an important role in maintaining the basal vascular tone and homeostasis in the cardiovascular system. In the present study, the ET-1 gene was silenced by RNA interference, and the effects on lung cancer cell proliferation and tumor cell invasion were then detected by Cell Counting kit-8 and Transwell assays. In addition, the expression of apoptosis, growth and invasion-associated proteins, including RhoA/C, vascular endothelial growth factor, pigment epithelium-derived factor, AKT, E-cadherin and cyclooxygenase-2 was evaluated by western blotting upon silencing ET-1. In the present study, Endostar, a recombinant human endostatin injectable drug, was also used, and it was assessed whether the sensitivity of tumor cells to this drug could be increased by silencing ET-1. Both in vivo and in vivo tests were carried out in the present study. The experimental data indicated that ET-1 silencing can inhibit tumor cell proliferation and invasion, particularly in the presence of Endostar.

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The effect of RhoC siRNA on the invasiveness and proliferation of human cervical cancer cell line SiHa cells

Cited by 6 publications

References 17 publications

Notch1 regulates the functional contribution of RhoC to cervical carcinoma progression

Notch1 regulates the functional contribution of RhoC to cervical carcinoma progression

Nuclear expression of Rac1 in cervical premalignant lesions and cervical cancer cells

Effects of silencing endothelin-1 on invasion and vascular formation in lung cancer

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