Long non-coding RNA LINC01963 inhibits progression of pancreatic carcinoma by targeting miR-641/TMEFF2

Li, Kailiang; Han, Hui; Gu, Wenjing; Cao, Chunyuan; Zheng, Peng‐Yuan

doi:10.1016/j.biopha.2020.110346

Cited by 22 publications

(16 citation statements)

References 21 publications

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“…The study also claimed that the experimental overexpression of TMEFF2 reduced phosphorylation of RAS, RAF, MEK and ERK in both AsPC1 and Panc1 cells. The onco-suppressive role of TMEFF2 in pancreatic cancer was also observed by Li et al [60] (the study reports positive regulation of TMEFF2 by LINC01963, LINC01963…”

Section: Proposed Functionssupporting

confidence: 70%

“…The study also claim experimental overexpression of TMEFF2 reduced phosphorylation of RAS, RAF, MEK both AsPC1 and Panc1 cells. The onco-suppressive role of TMEFF2 in pancreatic can observed by Li et al [60] (the study reports positive regulation of TMEFF2 by LINC01963 ⟞ miR-641 ⟞ TMEFF2). Fan et al [61] presented similar findings, wh overexpression led to an increase in apoptosis and a decrease in proliferation, cell m invasion capacities of the lung cancer cell line A549.…”

Section: Proposed Functionsmentioning

confidence: 85%

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TMEFF2: A Transmembrane Proteoglycan with Multifaceted Actions in Cancer and Disease

Masood

Grimm

El‐Bahrawy

et al. 2020

Cancers

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Transmembrane protein with an EGF-like and two Follistatin-like domains 2 (TMEFF2) is a 374-residue long type-I transmembrane proteoglycan which is proteolytically shed from the cell surface. The protein is involved in a range of functions including metabolism, neuroprotection, apoptosis, embryonic development, onco-suppression and endocrine function. TMEFF2 is methylated in numerous cancers, and an inverse correlation with the stage, response to therapy and survival outcome has been observed. Moreover, TMEFF2 methylation increases with breast, colon and gastric cancer progression. TMEFF2 is methylated early during oncogenesis in breast and colorectal cancer, and the detection of methylated free-circulating TMEFF2 DNA has been suggested as a potential diagnostic tool. The TMEFF2 downregulation signature equals and sometimes outperforms the Gleason and pathological scores in prostate cancer. TMEFF2 is downregulated in glioma and cotricotropinomas, and it impairs the production of adrenocorticotropic hormone in glioma cells. Interestingly, through binding the amyloid β protein, its precursor and derivatives, TMEFF2 provides neuroprotection in Alzheimer’s disease. Despite undergoing extensive investigation over the last two decades, the primary literature regarding TMEFF2 is incoherent and offers conflicting information, in particular, the oncogenic vs. onco-suppressive role of TMEFF2 in prostate cancer. For the first time, we have compiled, contextualised and critically analysed the vast body of TMEFF2-related literature and answered the apparent discrepancies regarding its function, tissue expression, intracellular localization and oncogenic vs. onco-suppressive role.

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Section: Proposed Functionssupporting

confidence: 70%

Section: Proposed Functionsmentioning

confidence: 85%

TMEFF2: A Transmembrane Proteoglycan with Multifaceted Actions in Cancer and Disease

Masood

Grimm

El‐Bahrawy

et al. 2020

Cancers

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“…At present, increasing evidence has shown that lncRNAs, which could act as competing endogenous RNA (ceRNA), play a crucial role in the occurrence and progression of malignant tumors via competitively binding to microRNAs (miRNAs) to regulate the expression of target mRNAs, and their aberrant expression are usually closely related to the proliferation, invasion, metastasis, and chemoresistance of tumor cells 6 – 8 . For instance, lncRNA LINC01963 increases TMEFF2 expression to inhibit the progression of pancreatic carcinoma cells via targeting miR-641 9 . LncRNA TALC promotes the expression of O6-methylguanine DNA methyltransferase (MGMT) by competitively binding miR-20b to activate the c-MET/STAT3/p300 axis, which leads to temozolomide (TMZ) resistance in glioblastoma 10 .…”

Section: Introductionmentioning

confidence: 99%

DLX6-AS1 activated by H3K4me1 enhanced secondary cisplatin resistance of lung squamous cell carcinoma through modulating miR-181a-5p/miR-382-5p/CELF1 axis

Zhao

Wang

Zhu

et al. 2021

Sci Rep

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Cisplatin (CDDP) based chemotherapy is widely used as the first-line strategy in treating non-small cell lung cancer (NSCLC), especially lung squamous cell carcinoma (LUSC). However, secondary cisplatin resistance majorly undermines the cisplatin efficacy leading to a worse prognosis. In this respect, we have identified the role of the DLX6-AS1/miR-181a-5p/miR-382-5p/CELF1 axis in regulating cisplatin resistance of LUSC. qRT-PCR and Western blot analysis were applied to detect gene expression. Transwell assay was used to evaluate the migration and invasion ability of LUSC cells. CCK-8 assay was used to investigate the IC50 of LUSC cells. Flow cytometry was used to test cell apoptosis rate. RNA pull-down and Dual luciferase reporter gene assay were performed to evaluate the crosstalk. DLX6-AS1 was aberrantly high expressed in LUSC tissues and cell lines, and negatively correlated with miR-181a-5p and miR-382-5p expression. DLX6-AS1 expression was enhanced by H3K4me1 in cisplatin resistant LUSC cells. Besides, DLX6-AS1 knockdown led to impaired IC50 of cisplatin resistant LUSC cells. Furthermore, DLX6-AS1 interacted with miR-181a-5p and miR-382-5p to regulate CELF1 expression and thereby mediated the cisplatin sensitivity of cisplatin resistant LUSC cells. DLX6-AS1 induced by H3K4me1 played an important role in promoting secondary cisplatin resistance of LUSC through regulating the miR-181a-5p/miR-382-5p/CELF1 axis. Therefore, targeting DLX6-AS1 might be a novel way of reversing secondary cisplatin resistance in LUSC.

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“…For example, Kong et al indicated that miR-641 was under-expressed in lung cancer cells, and repressed cell proliferation [ 19 ]. In the study of Li and his colleagues, we found the cancer-promoting role of miR-641 in pancreatic cancer by associating with LINC01963 [ 20 ]. Stromal interaction molecule 1 (STIM1), an important factor in regulating calcium channels, can dramatically affect intracellular Ca 2+ [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

Zhang

2021

BMC Cardiovasc Disord

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Background Atherosclerosis (AS) is a primary cause of coronary heart and vascular diseases. Long non-coding RNAs (lncRNAs) are indicated to regulate AS progression. This study aimed to reveal the biological roles of lncRNA myocardial infarction associated transcript (MIAT) in oxidized low-density lipoprotein (ox-LDL)-induced human vascular smooth muscle cells (VSMCs). Methods The RNA levels of MIAT, microRNA-641 (miR-641) and stromal interaction molecule 1 (STIM1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels were determined by western blot analysis. Cell proliferation was assessed by cell colony formation and DNA content quantitation assays. Cell migration and invasion were demonstrated by wound-healing and transwell assays. The putative binding relationships between miR-641 and MIAT or STIM1 were predicted by starbase online database, and identified by dual-luciferase reporter and RNA immunoprecipitation assays. Results MIAT and STIM1 expression were substantially upregulated, whereas miR-641 expression was downregulated in ox-LDL-induced VSMCs compared with control groups. Functionally, MIAT silencing attenuated ox-LDL-induced cell proliferation, migration and invasion in VSMCs; however, these effects were impaired by miR-641 inhibitor. STIM1 overexpression also restrained miR-641-mediated impacts on cell proliferation and metastasis under ox-LDL. Mechanistically, MIAT acted as a sponge for miR-641, and miR-641 was associated with STIM1. Conclusions MIAT silencing hindered ox-LDL-induced cell proliferation, migration and invasion by downregulating STIM1 expression through binding to miR-641 in VSMCs. The mechanism provided us with a new target for AS therapy.

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Long non-coding RNA LINC01963 inhibits progression of pancreatic carcinoma by targeting miR-641/TMEFF2

Cited by 22 publications

References 21 publications

TMEFF2: A Transmembrane Proteoglycan with Multifaceted Actions in Cancer and Disease

TMEFF2: A Transmembrane Proteoglycan with Multifaceted Actions in Cancer and Disease

DLX6-AS1 activated by H3K4me1 enhanced secondary cisplatin resistance of lung squamous cell carcinoma through modulating miR-181a-5p/miR-382-5p/CELF1 axis

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

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