Lentivirus-mediated Silencing of Rhomboid Domain Containing 1 Suppresses Tumor Growth and Induces Apoptosis in Hepatoma HepG2 Cells

Liu, Xue-Ni; Tang, Zisheng; Zhang, Yi; Pan, Qingchun; Chen, Xiaohua; Yu, Yongsheng; Zang, Guoqing

doi:10.7314/apjcp.2013.14.1.5

Cited by 15 publications

(13 citation statements)

References 27 publications

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“…Our results showed that the rate of lentivirus-mediated siRNA infection reached 80% which is much higher than that of liposome transfection we once used in our pretest. In previous studies, other target genes such as Med19 [ 26 ], RHBDD1 [ 27 ], and Wtp53-pPRIME-miR30 [ 28 ] were also specifically and effectively silenced by lentivirus-mediated siRNA, leading to significant antitumorigenesis effects in vivo or even in vitro . These results suggest that lentivirus-mediated siRNA system has good targeting ability and may serve as a potent therapeutic method for liver cancer.…”

Section: Discussionmentioning

confidence: 99%

Lentivirus-Mediated siRNA Targeting ER-αInhibits Tumorigenesis and Induces Apoptosis in Hepatocarcinoma Cells

Jiang

Cao

Bai

2015

BioMed Research International

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Background and Objectives. Estrogen receptor-α (ER-α) plays important roles in hepatocarcinogenesis. Recent studies have shown that ER-α could lead to cell cycle progression or inhibition of apoptosis. To better understand the role of ER-α, RNA interference (RNAi) was used to inhibit ER-α expression in the human hepatocellular carcinoma (HCC) cells. Methods. Lentivirus-mediated ER-α small interfering RNA (siRNA) was transfected into HCC cells Hep3B. ER-α expression was monitored by real-time polymerase chain reaction (PCR) and western blot. Cell proliferation, apoptosis, and invasion were examined by methyl thiazol tetrazolium (MTT), flow cytometry (FCM), and invasion assay, respectively. Results. ER-α siRNA efficiently downregulated the expression of ER-α in Hep3B cells at both mRNA and protein levels in a time-dependent manner. ER-α siRNA also inhibited cell proliferation and reduced cell invasion (compared with other groups, P < 0.05, resp.). Furthermore, knockdown of ER-α slowed down the cell population at S phase and increased the rate of apoptosis (P < 0.05, resp.). Conclusion. ER-α knockdown suppressed the growth of HCC cells. Thus, ER-α may play a very important role in carcinogenesis of HCC and its knockdown may offer a new potential gene therapy approach for human liver cancer in the future.

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Section: Discussionmentioning

confidence: 99%

Lentivirus-Mediated siRNA Targeting ER-αInhibits Tumorigenesis and Induces Apoptosis in Hepatocarcinoma Cells

Jiang

Cao

Bai

2015

BioMed Research International

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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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“…However, it remains unclear as to whether the rhomboid protease family is involved in CRC progression. A previous study in hepatoma cells suggested that RHBDD1 may be a positive regulator for HCC cell growth and apoptosis using recombinant lentivirus-mediated silencing of RHBDD1 in HepG2 cells (17). It is therefore conceivable that RHBDD1 has a similar, essential role in CRC tumorigenesis.…”

Section: Discussionmentioning

confidence: 98%

“…RHBDD1 exhibited a proteolytic activity in the tumor suppressor activated pathway-6, in both HCT116 and RKO colon cancer cells (15). Downregulation of RHBDD1 also demonstrated the ability to suppress proliferation and colony formation capability of HepG2 hepatocellular carcinoma cells (17). However, the precise function of RHBDD1 in CRC progression remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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

Han

Bai²,

Yao

et al. 2012

Molecular Medicine Reports

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Rhomboid domain containing 1 (RHBDD1), is a member of the rhomboid protease family, which has a pivotal role in the progression of numerous severe malignancies. However, its role in colorectal carcinoma (CRC) remains to be elucidated. In the present study, RHBDD1 was shown to be widely expressed in CRC cell lines. Lentivirus-mediated RNA interference was employed to knockdown RHBDD1 expression in RKO CRC cells. Functional analyses indicated that depletion of RHBDD1 expression resulted in significantly reduced CRC cell proliferation and colony formation, and induced a G0/G1 phase cell cycle arrest. The findings of the present study suggest that RHBDD1 may contribute to CRC tumorigenesis and serve as a potential therapeutic target in human CRC.

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Lentivirus-mediated Silencing of Rhomboid Domain Containing 1 Suppresses Tumor Growth and Induces Apoptosis in Hepatoma HepG2 Cells

Cited by 15 publications

References 27 publications

Lentivirus-Mediated siRNA Targeting ER-αInhibits Tumorigenesis and Induces Apoptosis in Hepatocarcinoma Cells

Lentivirus-Mediated siRNA Targeting ER-αInhibits Tumorigenesis and Induces Apoptosis in Hepatocarcinoma Cells

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

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

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