Knockdown of RHOC by shRNA suppresses invasion and migration of cholangiocellular carcinoma cells via inhibition of MMP2, MMP3, MMP9 and epithelial-mesenchymal transition

Yang, Huiling; Liang, Jun; Zhou, Jiupeng; Mi, Jianqiang; Ma, Ke; Fan, Yangwei; Ning, Jing; Wang, Chuying; Wei, Xin; Li, Enxiao

doi:10.3892/mmr.2016.5170

Cited by 25 publications

(14 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The interaction of FMNL-3 with RhoC was seen to lead to increased MMP2, MMP9 and VEGF, consequently leading to increased invasion in colon cancer cell lines [69]. The knockdown of RhoC in cholangiocellular carcinoma cells on the other hand, resulted in the suppression of invasion and migration [70]. On similar lines, YMO1, a protein belonging to the Yurt and mosaic family, was seen to reduce the invasion and metastatic ability of hepatocellular carcinoma cells, by targeting RhoC [71].…”

Section: Introductionmentioning

confidence: 99%

RhoC: a fascinating journey from a cytoskeletal organizer to a Cancer stem cell therapeutic target

Thomas

Pranatharthi

Ross

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Tumor heterogeneity results in differential response to therapy due to the existence of plastic tumor cells, called cancer stem cells (CSCs), which exhibit the property of resistance to therapy, invasion and metastasis. These cells have a distinct, signaling network active at every stage of progression. It is difficult to envisage that the CSCs will have a unique set of signaling pathways regulating every stage of disease progression. Rather, it would be easier to believe that a single pivotal pathway having significant contribution at every stage, which can further turn on a battery of signaling mechanisms specific to that stage, would be instrumental in regulating the signaling network, enabling easy transition from one state to another. In this context, we discuss the role of RhoC which has contributed to several phenotypes during tumor progression. RhoC (Ras homolog gene family member C) has been widely reported to regulate actin organization. It has been shown to impact the motility of cancer cells, resultantly affecting invasion and metastasis, and has contributed to carcinoma progression of the breast, pancreas, lung, ovaries and cervix, among several others. The most interesting finding has been its indispensable role in metastasis. Also, it has the ability to modulate various other phenotypes like angiogenesis, motility, invasion, metastasis, and anoikis resistance. These observations suggest that RhoC imparts the plasticity required by tumor cells to exhibit such diverse functions based on microenvironmental cues. This was further confirmed by recent reports which show that it regulates cancer stem cells in breast, ovary and head and neck cancers. Studies also suggest that the inhibition of RhoC results in abolition of advanced tumor phenotypes. Our review throws light on how RhoC, which is capable of modulating various phenotypes may be the apt core signaling candidate regulating disease progression. Additionally, mice studies show that RhoC is not essential for embryogenesis, giving scope for its development as a possible therapeutic target. This review thus stresses on the need to understand the protein and its functioning in greater detail to enable its development as a stem cell marker and a possible therapeutic target .

show abstract

Section: Introductionmentioning

confidence: 99%

RhoC: a fascinating journey from a cytoskeletal organizer to a Cancer stem cell therapeutic target

Thomas

Pranatharthi

Ross

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

show abstract

“… 19 , 20 We also provided evidence suggesting that the mechanism underlying the aforementioned effects was related to the inhibition of expression of MMP2, which is known to play a major role in tumor invasion and metastasis by proteolyzing the extracellular matrix. 21 , 22 These results indicated that the inhibition of cell proliferation, invasion, and migration in response to siRNA-RPN2 treatment may be mediated via the regulation of caspase-3, caspase-9, E-cadherin, and MMP2. PI3K/AKT signaling plays crucial roles in cell proliferation, migration, and invasion of human NPC.…”

Section: Discussionmentioning

confidence: 85%

Downregulation of ribophorin II suppresses tumor growth, migration, and invasion of nasopharyngeal carcinoma

Hong

et al. 2018

OTT

View full text Add to dashboard Cite

BackgroundIt has been reported that ribophorin II (RPN2) expression is increased in many cancers, but the role of RPN2 in nasopharyngeal carcinoma (NPC) remains unclear.Patients and methodsThis study found that the expression of RPN2 is increased dramatically in NPC tissues of patients compared with that in the adjacent normal tissues. This study attempted at understanding the effect of siRNA-RPN2 treatment on the migration and invasion of NPC cell lines CNE2 and HNE1.ResultsRT-PCR and Western blotting showed that RPN2 was highly expressed in CNE2 and HNE1 cells. siRNA-RPN2 treatment significantly inhibited cell viability at 24 and 48 h compared with the control group. Results of the transwell assay showed that, compared to the control groups, migration and invasion of the cells treated with siRNA-RPN2 decreased markedly. In addition, compared to the control groups, caspase-3, caspase-9, and E-cadherin expression levels increased and MMP 2 expression decreased significantly in the siRNA-RPN2-treated group. Phosphorylation of AKT and PI3K was also inhibited after siRNA-RPN2 treatment.ConclusionsiRNA-RPN2 can effectively inhibit the invasion and migration of human NPC cells via AKT/PI3K signaling. This can serve as a novel strategy for NPC treatment.

show abstract

“…Recent studies demonstrated that SPOCK1 regulates the EMT process during cancer metastasis ( 12 , 13 , 26 ). MMP3 and MMP9 are two mesenchymal markers that promote EMT and distant metastasis ( 27 ). In a previous study, SPOCK1 knockdown in PC3 cells significantly inhibited cell invasion and migration via downregulation of MMP3 and MMP9 ( 12 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑155‑5p inhibits the invasion and migration of prostate cancer cells by targeting SPOCK1

Yao

Zeng

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

The aim of the present study was to determine the effect of microRNA (miR)-155-5p on the expression of testican-1 (SPOCK1) and the invasion and migration of prostate cancer cells in vitro . Bioinformatics analysis and molecular biology assays revealed that SPOCK1 may be a direct target gene of miR-155-5p. In addition, a negative correlation was identified between SPCOK1 and miR-155-5p expression in prostate tumor tissues and cell lines. miR-155-5p mimic transfection inhibited SPOCK1 expression in PC3 cells and decreased cell migration and invasion abilities, while the expression of vimentin, N-cadherin, E-cadherin, β-catenin, matrix metalloproteinase (MMP)3 and MMP9 was upregulated. In summary, SPOCK1 was found to be a target gene of miR155-5p in prostate cancer, and miR-155-5p acts as a tumor-suppressor gene and may inhibit SPOCK1-mediated prostate cancer progression.

show abstract

Knockdown of RHOC by shRNA suppresses invasion and migration of cholangiocellular carcinoma cells via inhibition of MMP2, MMP3, MMP9 and epithelial-mesenchymal transition

Cited by 25 publications

References 33 publications

RhoC: a fascinating journey from a cytoskeletal organizer to a Cancer stem cell therapeutic target

RhoC: a fascinating journey from a cytoskeletal organizer to a Cancer stem cell therapeutic target

Downregulation of ribophorin II suppresses tumor growth, migration, and invasion of nasopharyngeal carcinoma

MicroRNA‑155‑5p inhibits the invasion and migration of prostate cancer cells by targeting SPOCK1

Contact Info

Product

Resources

About