Long noncoding RNA GMAN promotes hepatocellular carcinoma progression by interacting with eIF4B

Xu, Jianbo; Lu, Yijun; Liu, Qiaoyu; Xia, Anliang; Zhao, Jian; Xu, Xiaoliang; Sun, Qing‐Fu; Qi, Fuzhen; Sun, Beicheng

doi:10.1016/j.canlet.2019.12.032

Cited by 36 publications

(37 citation statements)

References 44 publications

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“…It is found that lncRNA has a great influence on the occurrence and development of liver cancer, laryngeal cancer, lung cancer and gastric cancer. LncRNA GMAN could interact with eIF4B and inhibited cancer cell apoptosis, thus promoted the survival and invasion of hepatocellular carcinoma [27]. In addition, LINC00460 acted as a sponge of miR-485 regulating Raf1, which facilitated proliferation, migration, invasion and EMT in papillary thyroid cancer [28].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

et al. 2020

Bioscience Reports

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Objective: To investigate the specific function of long non-coding RNA HAL in serous ovarian cancer (SOC) and to further clarify the regulation of HAL on EMT pathway. Materials and methods: The expression of HAL and TWIST1 was detected by qRT-PCR. CCK8 assay, wound healing assay, transwell assay and flow cytometry were used to detect the HAL function on proliferation, migration, invasion and apoptosis in SOC cells. Western blot was used to calculate protein level of Vimentin, N-cadherin and E-cadherin. The effect of HAL on tumorigenesis of SOC was confirmed by xenograft nude mice model. Results: HAL was significantly decreased in SOC tissues and cells. Overexpression of HAL inhibited the proliferation, migration and invasion of SKOV3 cells, but promoted apoptosis. Furthermore, overexpression of HAL decreased the mRNA and protein levels of TWIST1 via a binding between HAL and TWIST1. Forced expression of TWIST1 reversed the inhibitory role of HAL on SOC cells’ migration and invasion. The in vivo tumor growth assay showed that HAL suppressed SOC tumorigenesis with inhibiting EMT pathway. Conclusions: Our research emphasized HAL acting as a tumor-inhibiting gene by regulating EMT signaling pathway, thus providing some novel experimental basis for clinical treatment of SOC.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

et al. 2020

Bioscience Reports

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“…Up-regulation of c-myc driven by ARAP1-AS1 facilitates the development and progression of cervical cancer [16]. Another lncRNA GMAN is shown to directly interact with EIF4b and promote its phosphorylation and stability [17]. As a result, the translation of several anti-apoptosis-related proteins was enhanced.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA RP11-284P20.2 promotes cell proliferation and invasion in hepatocellular carcinoma by recruiting EIF3b to induce c-met protein synthesis

et al. 2020

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A newly identified lncRNA designated as RP11-284P20.2 has been identified to be up-regulated in hepatocellular carcinoma (HCC), but its role in HCC remain poorly understood. Quantitative PCR and immunocytochemical analysis were performed using the HCC tissues to identify the potential interaction partners of RP11-284P20.2. Moreover, RP11-284P20.2 was knocked down in HCC cell lines, HepG2 and SMMC7721, to investigate the influence of this lncRNA on cell growth properties. Additionally, RNA fluorescence in situ hybridization and immunofluorescence, RNA immunoprecipitation, and RNA pull-down assays were performed to determine the interaction of RP11-284P20.2 with c-met mRNA and eukaryotic translation initiation factor 3b (EIF3b). Silencing RP11-284P20.2 inhibited cell viability, migration, invasion, and colony formation, and increased apoptosis. Overexpression of c-met abolished these effects of RP11-284P20.2 in HCC cells. Histopathological examination showed that HCC tissues with high RP11-284P20.2 expression had higher c-met protein level than that in HCC tissues with low RP11-284P20.2 expression. However, there was no positive correlation between the expression levels of RP11-284P20.2 and c-met mRNA. RP11-284P20.2 knockdown led to a decease in c-met protein expression level, but did not affect the c-met mRNA expression level. These data suggest that RP11-284P20.2 regulates c-met protein expression level, which is independent of c-Met mRNA expression level. It was also confirmed that RP11-284P20.2 has high affinity toward both c-met mRNA and EIF3b protein, and hence RP11-284P20.2 probably recruits EIF3b protein to c-met mRNA and further facilitates its translation. RP11-284P20.2 promotes cell proliferation and invasion in hepatocellular carcinoma by recruiting EIF3b to induce c-met protein synthesis.

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“…Western blotting assays were conducted as previously reported 18 . The primary antibodies are as follows PR55α(1/1000, A2185, Abclonal, China), AKT(1/1000, A17909, Abclonal, China), p-AKT-T308(1/1000, AP0304, Abclonal, China), P-AKT-S473 (1/1000, AP0140, Abclonal, China), ERK1/2(1/1000, A4782, Abclonal, China) and p-ERK1/2-T202/Y204(1/1000, AP0472, Abclonal, China).…”

Section: Western Blottingmentioning

confidence: 99%

Loss of PR55α promotes proliferation and metastasis by activating MAPK/AKT signaling in hepatocellular carcinoma

JiangSheng¹,

Chen

JingQi

et al. 2021

Preprint

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Background: PR55α plays important roles in oncogenesis and progression of numerous malignancies. However, its role in hepatocellular carcinoma (HCC) is unclear. Methods: PR55α expressions in HCC tissues and paired healthy liver samples were detected using Western blot and tissue microarray immunohistochemistry. We knocked down the expression of PR55α in SMMC-7721 and LM3 cell lines via small interfering and lentivirus. In vitro cell counting, colony formation, migration and invasion assays were performed along with in vivo xenograft implantation and lung metastases experiments. The potential mechanisms involving target signal pathways were investigated by RNA-sequencing.Results: PR55α expression level was suppressed in HCC tissues in comparison to healthy liver samples and was indicative of poorer prognosis. Knockdown of PR55α significantly promoted cell proliferation and migration, induced repression of the cell cycle progression and apoptosis in vitro while accelerating in vivo HCC growth and metastasis. Mechanistic analysis indicated that PR55α silencing was involved with MAPK/AKT signal pathway activation and resulted in increased phosphorylation of both AKT and ERK1/2.Conclusion: This study identifies PR55α to be a candidate novel therapeutic target in the treatment of HCC.

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Long noncoding RNA GMAN promotes hepatocellular carcinoma progression by interacting with eIF4B

Cited by 36 publications

References 44 publications

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

Long non-coding RNA RP11-284P20.2 promotes cell proliferation and invasion in hepatocellular carcinoma by recruiting EIF3b to induce c-met protein synthesis

Loss of PR55α promotes proliferation and metastasis by activating MAPK/AKT signaling in hepatocellular carcinoma

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