Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway

Wang, C; Mao, Zheying; Wang, L; Wu, Guohong; Zhang, F H; Wang, D Y; Shi, Jiahong

doi:10.4149/neo_2017_510

Cited by 54 publications

(48 citation statements)

References 20 publications

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“…For instance, the response rate to gemcitabine‐based chemotherapy was 10.7% for pancreatic cancer patients with high MALAT1 expression, but 41.1% for gemcitabine‐based chemotherapy in patients with low MALAT1 expression. The progression‐free survival of patients with high and low expression levels of MALAT1 was 3.0 and 3.7 months (Wang, Mao et al, ). MALAT1 overexpression was associated with poor recurrence‐free survival in tamoxifen‐treated estrogen receptor (ER)‐positive breast cancer patients (Huang, Chi et al, ).…”

Section: Malat1 As a Biomarkermentioning

confidence: 99%

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

Chen

Huang

et al. 2018

Journal Cellular Physiology

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. MALAT1 is involved in regulating multiple cell behaviors, such as proliferation, apoptosis, differentiation, migration, epithelial-mesenchymal transition, autophagy, and morphological maintenance. Extensive evidence show that MALAT1 plays critical roles in the physiopathological process of embryo implantation, angiogenesis, tissue inflammation, tumor progression, liver fibrosis, cardiovascular remodeling, and diabetes progression by regulating gene transcription, forming RNA-protein complexes with proteins as a structural component, regulating protein activity, assisting protein localization, mediating epigenetic changes, or by acting as a competing endogenous RNA. Furthermore, MALAT1 can affect the sensitivity of chemotherapy and radiotherapy; therefore, it could be used as a potential drug target for chemotherapy and radiotherapy sensitization. The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion. Therefore, MALAT1 can be used as a biomarker for early diagnosis, severity assessment, or prognostic assessment. This review outlines the current understanding of the biological role and function of MALAT1. In the meantime, we have summarized the mechanisms involved in the reulation of MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.

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Section: Malat1 As a Biomarkermentioning

confidence: 99%

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

Chen

Huang

et al. 2018

Journal Cellular Physiology

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“…Few studies have reported a deregulation of lncRNA in iCCA . As an example, oncogenic metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) lncRNA was shown to promote proliferation and invasion of CCA cell lines by activating the phosphoinositide 3‐kinase/protein kinase B signaling pathway .…”

Section: Discussionmentioning

confidence: 99%

A novel transforming growth factor beta‐induced long noncoding RNA promotes an inflammatory microenvironment in human intrahepatic cholangiocarcinoma

Merdrignac

Angenard

Allain

et al. 2018

Hepatology Communications

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Intrahepatic cholangiocarcinoma (iCCA) is a deadly liver primary cancer associated with poor prognosis and limited therapeutic opportunities. Active transforming growth factor beta (TGFβ) signaling is a hallmark of the iCCA microenvironment. However, the impact of TGFβ on the transcriptome of iCCA tumor cells has been poorly investigated. Here, we have identified a specific TGFβ signature of genes commonly deregulated in iCCA cell lines, namely HuCCT1 and Huh28. Novel coding and noncoding TGFβ targets were identified, including a TGFβ‐induced long noncoding RNA (TLINC), formerly known as cancer susceptibility candidate 15 (CASC15). TLINC is a general target induced by TGFβ in hepatic and nonhepatic cell types. In iCCA cell lines, the expression of a long and short TLINC isoform was associated with an epithelial or mesenchymal phenotype, respectively. Both isoforms were detected in the nucleus and cytoplasm. The long isoform of TLINC was associated with a migratory phenotype in iCCA cell lines and with the induction of proinflammatory cytokines, including interleukin 8, both in vitro and in resected human iCCA. TLINC was also identified as a tumor marker expressed in both epithelial and stroma cells. In nontumor livers, TLINC was only expressed in specific portal areas with signs of ductular reaction and inflammation. Finally, we provide experimental evidence of circular isoforms of TLINC, both in iCCA cells treated with TGFβ and in resected human iCCA. Conclusion: We identify a novel TGFβ‐induced long noncoding RNA up‐regulated in human iCCA and associated with an inflammatory microenvironment. (Hepatology Communications 2018;2:254‐269)

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“…Previous research has shown that miR-22 regulates the activation of PI3K/Akt pathway (32). MALAT1 can promote the proliferation and epithelial-mesenchymal transition of cholangiocarcinoma and breast cancer cells by activating the PI3K/Akt signaling pathway (36,37). Therefore, we considered whether MALAT1 promoted the proliferation of RCC cells via the PI3K/Akt pathway.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA MALAT1 correlates with cell viability and mobility by targeting miR‑22‑3p in renal cell carcinoma via the PI3K/Akt pathway

Zhong

Ma²,

2018

Oncol Rep

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Renal cell carcinoma (RCC) is one of the most common types of cancer of the urinary tract in the world. Long non-coding RNA MALAT1 (lncR-MALAT1) is upregulated in RCC and is associated with the proliferation and migration of RCC. The present study aimed to investigate the regulating role of lncR-MALAT1 in RCC as well as the possible underlying mechanisms. The relative expression of MALAT1 and miR-22-3p in RCC tumor tissues and cell lines was detected by qRT-PCR. CCK-8 and wound healing assay were used to evaluate cell proliferation and migration ability. Western blot analysis was used to detect the expression of Ki-67, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase-3 (MMP-3), migration and invasion inhibitory protein (MIIP), p-PI3K and p-Akt. The relationship between MALAT1 and miR-22-3p was examined by bioinformatic prediction analysis and luciferase reporter assay. Immunofluorescence was used to detect the activation of Akt. MALAT1 was highly expressed and the expression of miR-22-3p was suppressed in RCC tissues and cell lines. ShRNA-mediated knockdown of MALAT1 significantly inhibited the viability and mobility of RCC cells in vitro and in vivo. Further experiments revealed that miR-22-3p was a target of MALAT1 and that miR-22-3p inhibitor abolished the effect of MALAT1 shRNA on cell proliferation, migration and inactivation of PI3K/AKT pathway. In conclusion, lncR-MALAT1 affected the proliferation and migration of RCC cells by targeting miR-22-3p through the inactivation of the PI3K/Akt signaling pathway.Abbreviations: MALAT1, metastasis-associated lung adenocarcinoma transcript 1; lncRNA, long non-coding RNA; RCC, renal cell carcinoma; miRNA, microRNA; MMP-3, matrix metaloproteinase-3; PCNA, proliferating cell nuclear antigen; MIIP, migration and invasion inhibitory protein; FBS, fetal bovine serum

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Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway

Cited by 54 publications

References 20 publications

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

A novel transforming growth factor beta‐induced long noncoding RNA promotes an inflammatory microenvironment in human intrahepatic cholangiocarcinoma

Long non‑coding RNA MALAT1 correlates with cell viability and mobility by targeting miR‑22‑3p in renal cell carcinoma via the PI3K/Akt pathway

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