RhoC Mediates Invasion and Migration of CaSki Cells Through the Rho-Associated Serine-Threonine Protein Kinase 1 Signaling Pathway

Chen, Rong; Cheng, Yuan; Zhang, Youyi; Li, Zijian; Geng, Li

doi:10.1097/igc.0000000000000053

Cited by 8 publications

(4 citation statements)

References 37 publications

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“…To identify the possible mechanism by which miR-217 elicited its effects in CC, the expression of ROCK1 was analyzed in CC tissues and cells. In line with the data of the previous study, ROCK1 was validated as an oncogene in CC cells ( 37 ). Further analysis revealed the presence of two conserved binding sites in the 3′UTR of ROCK1, and a dual-luciferase reporter assay indicated that ROCK1 was a target gene of miR-217.…”

Section: Discussionsupporting

confidence: 86%

MicroRNA‑217 functions as a tumor suppressor in cervical cancer cells through targeting Rho‑associated protein kinase 1

Dong

Wang

et al. 2018

Oncol Lett

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The abnormal expression of microRNAs (miRNAs/miRs) has been widely reported in various tumor types. miR-217 was demonstrated to be aberrantly expressed in a number of tumors, including pancreatic adenocarcinoma and osteosarcoma; however, its specific expression pattern has never been investigated in cervical cancer cells. Compared with normal control, the level of Rho-associated protein kinase 1 (ROCK1) expression was markedly increased in cervical cancer tissues and cells compared with that in non-cancerous tissues and cells. The expression of miR-217 was significantly reduced in cervical cancer tissues and cell lines. Overexpression of miR-217 could suppress colony formation and the cell invasion capacity of SiHa and HeLa cells. Flow cytometry indicated that miR-217 significantly increased cell apoptosis in SiHa and HeLa cells. Dual-luciferase reporter assays demonstrated that ROCK1 was a target gene of miR-217. In addition, overexpression of ROCK1 also led to an increased invasion capacity in SiHa cells, even when miR-217 was inhibited, indicating that the anti-invasive effects of miR-217 were mediated through ROCK1. In summary, the results of the present study indicated that miR-217 functions as a tumor suppressor in cervical cancer cells, primarily by targeting ROCK1.

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Section: Discussionsupporting

confidence: 86%

MicroRNA‑217 functions as a tumor suppressor in cervical cancer cells through targeting Rho‑associated protein kinase 1

Dong

Wang

et al. 2018

Oncol Lett

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“…RHOC belongs to RHO family proteins, which regulate extracellular stimuli-mediated signaling pathways that control numerous intracellular processes, including actin cytoskeletal organization, gene expression, invasion and cell cycle progression ( 22 , 29 – 31 ). RHOC has been characterized as an oncogenic kinase that promotes cancer cell proliferation, invasion and migration ( 32 – 34 ). High levels of RHOC activity are associated with metastatic lesions and a poor clinical outcome ( 35 , 36 ).…”

Section: Discussionmentioning

confidence: 99%

HOXD10 acts as a tumor-suppressive factor via inhibition of the RHOC/AKT/MAPK pathway in human cholangiocellular carcinoma

Yang

Zhou

et al. 2015

Oncology Reports

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HOXD10, a key regulator of cell-differentiated phenotype maintainence, has been demonstrated to be involved in the tumorigenesis of many human malignacies. However, the status of HOXD10 expression and its biological function in cholangiocellular carcinoma (CCC) remain to be clarified. In the present study, we investigated the clinical significance and biological functions of HOXD10 in CCC and found that the expression of HOXD10 and its downstream effector RHOC was significantly different in well-differentiated CCC tissues compared with poorly-differentiated lesions. We also observed a significant correlation between low HOXD10 and high RHOC expression levels and worse prognosis. The stable overexpression of HOXD10 by lentivirus vector significantly inhibited cell invasion partly by downregulating the expression of MMP2 and MMP9, and significantly increased early apoptosis in CCC cell lines and induced G1 phase cell cycle arrest, contributing to the inhibition of cell proliferation in vitro. Additionally, we demonstrated that the inactivation of the RHOC/AKT/MAPK pathway was involved in the tumor-suppressive functions of HOXD10 in CCC. These results suggested that HOXD10 may be a putative suppressor gene and can act as a prognostic marker and potentially a novel therapeutic target for CCC.

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“…Y-27632 inhibited ROCK1 in human cervical carcinoma (CaSki) cells with overexpressed RhoC that eventually led to decreases in the rate of invasiveness and migration. Blockage of the RhoC downstream signaling by small molecule inhibitors may represent a potent treatment strategy to inhibit tumor invasion and migration [170].…”

Section: Y-27632mentioning

confidence: 99%

Rho GTPases in Gynecologic Cancers: In-Depth Analysis toward the Paradigm Change from Reactive to Predictive, Preventive, and Personalized Medical Approach Benefiting the Patient and Healthcare

Žúbor

Daňková

Kolková

et al. 2020

Cancers

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Rho guanosine triphospatases (GTPases) resemble a conserved family of GTP-binding proteins regulating actin cytoskeleton dynamics and several signaling pathways central for the cell. Rho GTPases create a so-called Ras-superfamily of GTPases subdivided into subgroups comprising at least 20 members. Rho GTPases play a key regulatory role in gene expression, cell cycle control and proliferation, epithelial cell polarity, cell migration, survival, and apoptosis, among others. They also have tissue-related functions including angiogenesis being involved in inflammatory and wound healing processes. Contextually, any abnormality in the Rho GTPase function may result in severe consequences at molecular, cellular, and tissue levels. Rho GTPases also play a key role in tumorigenesis and metastatic disease. Corresponding mechanisms include a number of targets such as kinases and scaffold/adaptor-like proteins initiating GTPases-related signaling cascades. The accumulated evidence demonstrates the oncogenic relevance of Rho GTPases for several solid malignancies including breast, liver, bladder, melanoma, testicular, lung, central nervous system (CNS), head and neck, cervical, and ovarian cancers. Furthermore, Rho GTPases play a crucial role in the development of radio- and chemoresistance e.g. under cisplatin-based cancer treatment. This article provides an in-depth overview on the role of Rho GTPases in gynecological cancers, highlights relevant signaling pathways and pathomechanisms, and sheds light on their involvement in tumor progression, metastatic spread, and radio/chemo resistance. In addition, insights into a spectrum of novel biomarkers and innovative approaches based on the paradigm shift from reactive to predictive, preventive, and personalized medicine are provided.

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RhoC Mediates Invasion and Migration of CaSki Cells Through the Rho-Associated Serine-Threonine Protein Kinase 1 Signaling Pathway

Abstract: This study suggested that the activation of RhoC/ROCK1 signaling pathways is likely involved in the progression of cervical squamous cell carcinoma.

Cited by 8 publications

References 37 publications

MicroRNA‑217 functions as a tumor suppressor in cervical cancer cells through targeting Rho‑associated protein kinase 1

MicroRNA‑217 functions as a tumor suppressor in cervical cancer cells through targeting Rho‑associated protein kinase 1

HOXD10 acts as a tumor-suppressive factor via inhibition of the RHOC/AKT/MAPK pathway in human cholangiocellular carcinoma

Rho GTPases in Gynecologic Cancers: In-Depth Analysis toward the Paradigm Change from Reactive to Predictive, Preventive, and Personalized Medical Approach Benefiting the Patient and Healthcare

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