Lentivirus-mediated knockdown of rhomboid domain containing 1 inhibits colorectal cancer cell growth

Han, Jiazhen; Bai, Junchao; Yao, Yang; Yin, Hua; Gao, Wei; Liu, Aiguo; Liu, Fei; Ge, Haiyan; Liu, Zhongmin; Wang, Jinyi; Zhong, Li-Ye

doi:10.3892/mmr.2015.3365

Cited by 8 publications

(8 citation statements)

References 21 publications

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“…Rhomboid domain-containing protein 1 (RHBDD1), a new member of the Rhomboid family is highly responsible for the regulation of apoptosis cleaving pro-apoptotic Bcl-2 family protein BIK [14]. Related studies showed that RNA interference (RNA) mediated RHBDD1 silencing significantly suppressed cell proliferation and cell cycle progression in hepatocellular carcinoma [15], glioblastoma [16] and colorectal cancer [17]. Moreover, Zhang et al [18] demonstrated that RHBDD1 could promote tumor metastasis by promoting Wnt/β-catenin signaling and epithelial-mesenchymal transition in colorectal cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-924 as a tumor suppressor inhibits non-small cell lung cancer by inhibiting RHBDD1/Wnt/β-catenin signaling pathway

et al. 2020

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Background MiR-924 has been reported to be a tumor suppressor in hepatocellular carcinoma. However, the functions and mechanisms of miR-924 in non-small cell lung cancer (NSCLC) remain unclear. Methods The expression of miR-924 was determined in NSCLC tissues and cell lines using quantitative real time PCR. The Chi-squared test was used to evaluate the correlation between miR-924 levels and clinicopathological parameters in patients with NSCLC. Cell proliferation was assessed by CCK-8 assay. Cell migration and invasion were detected by transwell assay. The combination of miR-924 and RHBDD1 was analyzed via the luciferase reporter assay. The expression level of RHBDD1 was evaluated in lung cancer tissues using public microarray datasets form Oncomine and its prognostic value was assessed by Kaplan–Meier Plotter databases. A tumor xenograft mouse model was established to illustrate the effects of miR-924 on the tumorigenesis of NSCLC in vivo. Results In this study, we found miR-924 was strikingly decreased in NSCLC tissues and cell lines. Decreased miR-924 was closely correlated with advanced tumor-node-metastasis (TNM) stage and lymphatic metastasis in NSCLC patients. Noticeably, rhomboid domain-containing protein 1 (RHBDD1) was predicted and confirmed as a direct target of miR-924. Moreover, the expression level of RHBDD1 was significantly increased and inversely associated with prognosis using public microarray datasets form Oncomine and Kaplan–Meier Plotter databases. MiR-924 overexpression suppressed cell proliferation, migration and invasion. The in vivo experiments further demonstrated that miR-924 overexpression reduced NSCLC xenograft growth through inhibiting RHBDD1/Wnt/β-catenin signaling pathway. Conclusions In summary, these findings demonstrated that miR-924 blocked the progression of NSCLC by targeting RHBDD1 and miR-924/RHBDD1 axis might provide a novel therapeutic target for the treatment of NSCLC.

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Section: Introductionmentioning

confidence: 99%

MiR-924 as a tumor suppressor inhibits non-small cell lung cancer by inhibiting RHBDD1/Wnt/β-catenin signaling pathway

et al. 2020

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“…Emerging evidence indicates that silencing RHBDD1 suppresses cell growth and proliferation in hepatocellular carcinoma [13], glioblastoma [14] and colorectal cancer [15]. In breast cancer [16,17] and colorectal cancer cells [18], RHBDD1 has been shown to promote migration, invasion and EMT.…”

Section: Introductionmentioning

confidence: 99%

Silibinin suppresses epithelial–mesenchymal transition in human non-small cell lung cancer cells by restraining RHBDD1

Zhang

Wang

et al. 2020

Cell Mol Biol Lett

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Background: Rhomboid domain containing 1 (RHBDD1) plays a crucial role in tumorigenesis. Silibinin, which is a natural extract from milk thistle, has shown antitumor effects against various tumors. Here, we investigate whether silibinin affects the function of RHBDD1 in non-small cell lung cancer (NSCLC) cell proliferation, migration and invasion. Methods: The Oncomine database and an immunohistochemistry (IHC) assay were used to determine the RHBDD1 expression levels in lung cancer tissues. The associations between RHBDD1 and overall survival rate or clinicopathological parameters were respectively assessed using the Kaplan-Meier overall survival analysis or Chi-squared test. CCK-8 and Transwell assays were applied to analyze cell proliferation, migration and invasion. A549 cells were incubated with increasing concentrations of silibinin. RHBDD1 knockdown and overexpression were achieved via transfection with si-RHBDD1 or RHBDD1 overexpression plasmid, respectively. Western blotting was performed to measure the expressions of epithelialmesenchymal transition (EMT) markers. Results:We found that overexpression of RHBDD1 in lung cancer tissues correlates with a poor prognosis of survival. Clinical specimen analysis showed that upregulation of RHBDD1 correlates remarkably well with TNM stage and lymph node metastasis. Silibinin suppresses A549 cell proliferation, migration, invasion and EMT in a dose-dependent manner. Importantly, RHBDD1 was downregulated in silibinintreated A549 cells. RHBDD1 overexpression reversed the suppressive effects of silibinin on A549 cell proliferation, migration, invasion and EMT expression, while its knockdown enhanced them.Conclusions: These findings shown an anti-tumor impact of silibinin on NSCLC cells via repression of RHBDD1.

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“…By loss-of-function assay, we further demonstrated that knockdown of RHBDD1 significantly suppressed cell proliferation, migration, and invasion as well as induced cell cycle of G0/G1 arrest in glioma cells. In fact, RHBDD1 has been widely reported to be an oncogene in tumor cell proliferation and tumor metastasis, including breast cancer [10,40], renal cell carcinoma [14], colorectal cancer [8,30], and HCC [16]. Consistently, Wei et al [34] previously reported that silencing of RHBDD1 caused significant inhibition of cell cycle progression and cell proliferation in glioblastoma cells.…”

Section: Discussionmentioning

confidence: 80%

Effects of miR-211-3p/RHBDD1 axis on cell proliferation, cell cycle progression, and epithelial-mesenchymal transition in glioma

Chen¹,

Wang²,

Zhu³

et al. 2022

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This study was designed to elucidate the relationship of miR-211-3p and rhomboid domain containing 1 (RHBDD1) in glioma. Here, we first observed that miR-211-3p directly targets the 3′-UTR of RHBDD1 in glioma cells using dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blot analysis. Pearson's correlation analysis showed that miR-211-3p expression was negatively correlated with RHBDD1 expression in glioma tissues. CCK-8 assay, flow cytometry, and transwell assay were applied to assess cell proliferation, cell cycle distribution, migration, and invasion. The results showed that RHBDD1 knockdown inhibited cell proliferation, cell cycle G1/S transition, migration, and invasion in two glioma cell lines (U87 and . Knockdown of miR-211-3p obtained opposite results. Moreover, overexpression of RHBDD1 counteracted suppressive effects of miR-211-3p on glioma cells. Furthermore, decreased expression of CDK4, cyclin D1, N-cadherin, and vimentin as well as increased E-cadherin expression induced by miR-211-3p was reversed by RHBDD1 overexpression. Our results suggested that targeting miR-211-3p/RHBDD1 axis might be a novel effective therapeutic target for glioma treatment.

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Lentivirus-mediated knockdown of rhomboid domain containing 1 inhibits colorectal cancer cell growth

Cited by 8 publications

References 21 publications

MiR-924 as a tumor suppressor inhibits non-small cell lung cancer by inhibiting RHBDD1/Wnt/β-catenin signaling pathway

MiR-924 as a tumor suppressor inhibits non-small cell lung cancer by inhibiting RHBDD1/Wnt/β-catenin signaling pathway

Silibinin suppresses epithelial–mesenchymal transition in human non-small cell lung cancer cells by restraining RHBDD1

Effects of miR-211-3p/RHBDD1 axis on cell proliferation, cell cycle progression, and epithelial-mesenchymal transition in glioma

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