Long noncoding RNA MALAT1 inhibits the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis

Peng, Ning-Fu; He, Jingrong; Li, Jindu; Huang, Hao; Huang, WeiQiao; Liao, Ying‐Yang; Zhu, Shao‐Liang

doi:10.1186/s12935-020-01231-w

Cited by 63 publications

(44 citation statements)

References 49 publications

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“…Among these LncRNAs, MALAT1 has been commonly considered as a promising therapeutical target due to its well-conserved property between species [11,12]. MALAT1 has been found to inhibit the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis [13]. Besides, the relationship between MALAT1 and gynecological oncology has been gradually investigated.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MALAT1 Accelerates Cervical Carcinoma Proliferation by Suppressing miR-124 Expression in Cervical Tumor Cells

Tian

Wang

et al. 2021

Journal of Oncology

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Emerging studies have clarified the critical role of LncRNA MALAT1 in various pathological progressions. Here, we identified its positive relationship with cervical carcinoma proliferation. Cervical carcinoma has been considered as one of the most malignant tumors among female. Thus, our study was designed to investigate the underlying mechanism of LncRNA MALAT1 on cervical tumor cell proliferation. We observed that miR-124 was the potential target of LncRNA MALAT1 in cervical tumor cell lines (Hela, C-33A, Caski, and SiHa), the expression level of which is negatively correlated with LncRNA MALAT1 in cervical tumor cells, tissues of cervical patients, and mice. Gain- or loss-of-function analyses in cervical tumor cells have further verified the regulatory role of MALAT1 on miR-124. Additionally, the proliferation of cervical carcinoma was inhibited by miR-124 overexpression, whereas it was blocked by LV-MALAT1 transfection. In vivo assays, overexpression of miR-124, or knockdown of MALAT1 exhibited beneficial effects on tumor weight, size, and volume, together with elevating the survival rate, tightly related with the progression of cervical cancer. In conclusion, LncRNA MALAT1 disabled the effects of miR-124 as an inhibitory sponge, accelerating the progression of cervical carcinoma.

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Section: Introductionmentioning

confidence: 99%

LncRNA MALAT1 Accelerates Cervical Carcinoma Proliferation by Suppressing miR-124 Expression in Cervical Tumor Cells

Tian

Wang

et al. 2021

Journal of Oncology

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“…Our results are consistent with several recent studies of MALAT1 in HCC, confirming that MALAT1 plays an oncogenic role in HCC by promoting cell proliferation, migration, and invasion 41 – 44 . Other studies also found that MALAT1 can regulate apoptosis, autophagy, and inflammatory response of HCC cells, implying that MALAT1 may coordinate multiple aspects of cell features to promote HCC progress 45 , 46 . In our study, mascRNA was found to have similar roles as its parent RNA MALAT1.…”

Section: Discussionmentioning

confidence: 92%

mascRNA and its parent lncRNA MALAT1 promote proliferation and metastasis of hepatocellular carcinoma cells by activating ERK/MAPK signaling pathway

et al. 2021

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MALAT1-associated small cytoplasmic RNA (mascRNA) is a cytoplasmic tRNA-like small RNA derived from nucleus-located long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). While MALAT1 was extensively studied and was found to function in multiple cellular processes, including tumorigenesis and tumor progression, the role of mascRNA was largely unknown. Here we show that mascRNA is upregulated in multiple cancer cell lines and hepatocellular carcinoma (HCC) clinical samples. Using HCC cells as model, we found that mascRNA and its parent lncRNA MALAT1 can both promote cell proliferation, migration, and invasion in vitro. Correspondingly, both of them can enhance the tumor growth in mice subcutaneous tumor model and can promote metastasis by tail intravenous injection of HCC cells. Furthermore, we revealed that mascRNA and MALAT1 can both activate ERK/MAPK signaling pathway, which regulates metastasis-related genes and may contribute to the aggressive phenotype of HCC cells. Our results indicate a coordination in function and mechanism of mascRNA and MALAT1 during development and progress of HCC, and provide a paradigm for deciphering tRNA-like structures and their parent transcripts in mammalian cells.

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“…MALAT1 and NEAT1 have been widely studied non-coding RNAs, and some studies have demonstrated that they have clear correlations with various cancers such as hepatocellular carcinoma and lung cancer [ 30 – 33 ]. It has also been reported that MALAT1 can be used as ceRNA of miR-199a to promote the expression of ZHX1 , which in turn can regulate the proliferation of GBM cells [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of ceRNA network related to lincRNA in glioblastoma and prediction of clinical prognosis

Liu

Huang

et al. 2021

BMC Cancer

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Background Long intergenic non-coding RNAs (lincRNAs) are capable of regulating several tumours, while competitive endogenous RNA (ceRNA) networks are of great significance in revealing the biological mechanism of tumours. Here, we aimed to study the ceRNA network of lincRNA in glioblastoma (GBM). Methods We obtained GBM and normal brain tissue samples from TCGA, GTEx, and GEO databases, and performed weighted gene co-expression network analysis and differential expression analysis on all lincRNA and mRNA data. Subsequently, we predicted the interaction between lincRNAs, miRNAs, and target mRNAs. Univariate and multivariate Cox regression analyses were performed on the mRNAs using CGGA data, and a Cox proportional hazards regression model was constructed. The ceRNA network was further screened by the DEmiRNA and mRNA of Cox model. Results A prognostic prediction model was constructed for patients with GBM. We assembled a ceRNA network consisting of 18 lincRNAs, 6 miRNAs, and 8 mRNAs. Gene Set Enrichment Analysis was carried out on four lincRNAs with obvious differential expressions and relatively few studies in GBM. Conclusion We identified four lincRNAs that have research value for GBM and obtained the ceRNA network. Our research is expected to facilitate in-depth understanding and study of the molecular mechanism of GBM, and provide new insights into targeted therapy and prognosis of the tumour.

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Long noncoding RNA MALAT1 inhibits the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis

Cited by 63 publications

References 49 publications

LncRNA MALAT1 Accelerates Cervical Carcinoma Proliferation by Suppressing miR-124 Expression in Cervical Tumor Cells

LncRNA MALAT1 Accelerates Cervical Carcinoma Proliferation by Suppressing miR-124 Expression in Cervical Tumor Cells

mascRNA and its parent lncRNA MALAT1 promote proliferation and metastasis of hepatocellular carcinoma cells by activating ERK/MAPK signaling pathway

Comprehensive analysis of ceRNA network related to lincRNA in glioblastoma and prediction of clinical prognosis

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