Downregulation of ROS-FIG inhibits cell proliferation, colony-formation, cell cycle progression, migration and invasion, while inducing apoptosis in intrahepatic cholangiocarcinoma cells

Deng, Gang; Hu, Chenghuan; Zhu, Lei; Huang, Feizhou; Huang, Wei; Xu, Hongbo; Nie, Wei

doi:10.3892/ijmm.2014.1823

Cited by 14 publications

(11 citation statements)

References 25 publications

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“…In the present study, 20 We found that ROS1 knockdown mediated by specific shRNA transfection significantly reduced cell viability and inhibited colony formation of gastric cancer cells (BGC-823 and SGC-7901). Deng G et al have observed similar results in intrahepatic cholangiocarcinoma cells, 18 which are consistent with our studies. Cell cycle is a highly ordered process that tightly regulated by multiple cell cyclerelated regulators.…”

Section: Discussionsupporting

confidence: 93%

“…32,33 Deng G et al have demonstrated that ROS1 shRNA transfection inhibits the migration and invasion of intrahepatic cholangiocarcinoma cells. 18 Consistently, we found that ROS1 knockdown significantly reduced the migratory and invasive capabilities of gastric cancer cells. EMT has been demonstrated to be a major cause of cell migration and invasion.…”

Section: Discussionsupporting

confidence: 72%

“…17 Deng G et al demonstrated that downregulation of ROS1 using shRNA inhibited cell proliferation, migration and invasion and induced cell apoptosis in intrahepatic cholangiocarcinoma cells. 18 However, few studies have reported the effects of ROS1 on gastric cancer and investigated the precise mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

Jian¹,

Sun³

et al. 2019

OTT

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Objectives: Gastric cancer ranks the fourth most common cancer and the third leading cause of cancer mortality in the world. ROS proto-oncogene 1 (ROS1) is an oncogene and ROS1 rearrangement has been reported in many cancers. Our study aimed to investigate the potential function and the precise mechanisms of ROS1 in gastric cancer. Methods: In our study, the analysis of ROS1 expression and clinical pathologic factors of gastric cancer in gastric cancer using TCGA database demonstrated that ROS1 expression was elevated in gastric cancer and related to T, N, M and TNM staging. High expression of ROS1 predicted poor survival in patients with gastric cancer. Then, we measured ROS1 expression in four human gastric cancer cell lines and knocked down ROS1 expression in BGC-823 and SGC-7901 cells by specific shRNA transfection via Lipofectamine 2000. The effect of ROS1 knockdown on cell proliferation, cell cycle distribution, cell apoptosis and metastasis in vitro was evaluated by MTT, colony formation, flow cytometric analysis, wound healing and Transwell invasion assays. The levels of apoptosis-related proteins, EMT markers and the PI3K/Akt signaling pathway members were measured by Western blotting. Results: We demonstrated that shROS1 transfection markedly downregulated ROS1 expression in BGC-823 and SGC-7901 cells. Knockdown of ROS1 inhibited cell survival, clonogenic growth, migration, invasion and epithelial-mesenchymal transition (EMT), as well as induced cell cycle arrest and apoptosis in gastric cancer cells. Furthermore, ROS1 knockdown inhibited the phosphorylation of PI3K and Akt. Conclusion: Collectively, our data suggest that ROS1 may serve as a promising therapeutic target in gastric cancer treatment.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 72%

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<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

Jian¹,

Sun³

et al. 2019

OTT

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“…Notably, ROS can stimulate the expression of numerous metastatic factors, which leads to HCC cell migration and invasion (13,16). In addition, ROS production is an important etiological mechanism in PM 2.5 -induced tissue injury (17–19).…”

Section: Introductionmentioning

confidence: 99%

Atmospheric particulate matter2.5 promotes the migration and invasion of hepatocellular carcinoma cells

et al. 2017

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Epidemiological data has demonstrated that particulate matter (PM) with an aerodynamic diameter ≤ 2.5 µm (PM2.5) is associated with cancer incidence. However, the precise mechanisms underlying PM2.5-mediated hepatocellular carcinoma cancer (HCC) migration and invasion remain unclear. The aim of the present study was to explore the response of the HCC cell lines HepG2 and HuH-7 to PM2.5 exposure. The results revealed that PM2.5 treatment promoted the migration and invasion of HCC cells, in addition to increasing protein levels of matrix metalloproteinase (MMP)-13. Additionally, PM2.5 induced intracellular reactive oxygen species formation in HCC cells. Further investigation revealed that phosphorylation of RAC-alpha serine/threonine-protein kinase (AKT) increased in response to PM2.5 exposure in HCC cells, and the AKT antagonist LY294002 reduced PM2.5-induced migration, invasion and MMP-13 expression. In addition, the data from the present study demonstrated that high concentrations of PM2.5 decreased the proliferation of normal HL7702 hepatocyte cells and promoted apoptosis. These results indicate that the activation of AKT by PM2.5 results in MMP-13 overexpression, and stimulates HCC cell migration and invasion. In conclusion, the results from the present study demonstrate that PM2.5 promotes HCC development and elucidate a potential underlying molecular mechanism for this effect.

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“…Colony formation. Colony formation analysis was performed as described previously (36). Briefly, when the transfected cells were growing in the logarithmic phase they were trypsinized with 0.05% Trypsin-EDTA (Gibco; Thermo Fisher Scientific, Inc.) and seeded into 6-well plates at a density of 2,000 cells/well.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-181a promotes proliferation and inhibits apoptosis by suppressing CFIm25 in osteosarcoma

Zhu

Huang

Chong

et al. 2016

Molecular Medicine Reports

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MicroRNA-181a (miR-181a) is upregulated in osteosarcoma, and its overexpression promotes the proliferation and inhibits the apoptosis of osteosarcoma cells. However, the mechanism of miR‑181a as an oncogene remains to be fully elucidated in osteosarcoma. Cleavage factor (CF) Im25 links alternative polyadenylation to glioblastoma tumor suppression, however, its role in osteosarcoma has not been reported. In the present study, it was confirmed that the expression of miR‑181a was upregulated in osteosarcoma, and that silencing miR‑181a inhibited the proliferation and promoted the apoptosis of osteosarcoma cells. miRNAs are short non‑coding RNAs, which regulate target mRNAs by binding predominantly to the 3'untranslated region (3'UTR), inducing either translational repression or degradation of the target. In the present study, target genes of miR‑181a were screened using miRanda, which is a commonly used prediction algorithm. It was found that miR‑181a targeted the 3'UTR of CFIm25 mRNA. Subsequent experiments confirmed that miR‑181a downregulated the expression of CFIm25 in osteosarcoma cells. Finally, it was demonstrated that the CFIm25 protein was also downregulated in osteosarcoma tissues, and inhibited the proliferation and promoted the apoptosis of the cells. Elucidating the roles of miR‑181a and CFIm25 in osteosarcoma not only assists in further understanding the pathogenesis and progression of this disease, but also offers novel targets for effective therapies.

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Downregulation of ROS-FIG inhibits cell proliferation, colony-formation, cell cycle progression, migration and invasion, while inducing apoptosis in intrahepatic cholangiocarcinoma cells

Cited by 14 publications

References 25 publications

<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

Atmospheric particulate matter2.5 promotes the migration and invasion of hepatocellular carcinoma cells

MicroRNA-181a promotes proliferation and inhibits apoptosis by suppressing CFIm25 in osteosarcoma

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