LncRNA TUSC7 suppresses pancreatic carcinoma progression by modulating miR‐371a‐5p expression

Yue, Lei; Guo, Jing

doi:10.1002/jcp.28248

Cited by 24 publications

(17 citation statements)

References 33 publications

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“…According to bioinformatics analysis and experimental validation by dual-luciferase reporter assays, our findings suggest that CRART16 overexpression increased ERBB3 expression by binding to miR-371a-5p. Several previous studies have shown that miR-371a-5p contributes to the development and progression of different cancers, such as hepatocellular carcinoma (HCC) [35] and pancreatic carcinoma [36]. In this study, a rescue assay indicated that CRART16 overexpression-induced cetuximab resistance was partially counteracted by miR-371a-5p mimics, which suggested that CRART16 might also act through other mechanisms.…”

Section: Discussionmentioning

confidence: 51%

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

et al. 2020

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Background: Long noncoding RNAs (lncRNAs) have been shown to participate in multiple biological processes and confer drug resistance. However, it remains unclear whether lncRNAs are involved in conferring cetuximab resistance in colorectal cancer (CRC) cells.Methods: Cell Counting Kit-8 (CCK-8) assays were performed to assess the sensitivity of CRC cell lines to cetuximab treatment. -2 cells were stably transduced with cetuximab resistance-associated RNA transcript 16 (CRART16) or an empty vector using lentiviral infection; the cells were designated Caco-2-CRART16 and Caco-2-NC, respectively, and were analyzed with RNA sequencing (RNA-seq). Quantitative real-time PCR (qRT-PCR) was performed to investigate RNA expression. Flow cytometry and TUNEL assays were used to assess apoptosis levels induced by cetuximab. The cell cycle, stemness biomarkers and membrane proteins of CRC cells were assessed via flow cytometry. RNA fluorescence in situ hybridization (FISH) was used to examine CRART16 localization and expression. Bioinformatics analysis was performed to predict the potential mechanism of CRART16, which was further validated by a dual-luciferase reporter assay. Differences in measurement data were compared using Student's t test, one-way ANOVA followed by Dunnett's test and two-way ANOVA.

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Section: Discussionmentioning

confidence: 51%

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

et al. 2020

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“…Tumor suppressor candidate 7 ( TUSC7 ) expression was found down regulated in HCC, NSCLC, pancreatic carcinoma, colorectal cancer, glioma and other tumor types [111,112,113]. In HCC, it counteracts EMT and invasion capacity sponging miR-10a, a well-known upregulated miRNA in this type of carcinoma, increasing the expression of the anti-EMT EPHA4 [111].…”

Section: Anti-emt Lncrnasmentioning

confidence: 99%

“…In HCC, it counteracts EMT and invasion capacity sponging miR-10a, a well-known upregulated miRNA in this type of carcinoma, increasing the expression of the anti-EMT EPHA4 [111]. In other cell contexts, TUSC7 can function as ceRNA for other miRNAs which positively control EMT, like miR-211 and miR-371a-5p [113,114].…”

Section: Anti-emt Lncrnasmentioning

confidence: 99%

Long Noncoding RNA and Epithelial Mesenchymal Transition in Cancer

Gugnoni

Ciarrocchi

2019

IJMS

123

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Epithelial–mesenchymal transition (EMT) is a multistep process that allows epithelial cells to acquire mesenchymal properties. Fundamental in the early stages of embryonic development, this process is aberrantly activated in aggressive cancerous cells to gain motility and invasion capacity, thus promoting metastatic phenotypes. For this reason, EMT is a central topic in cancer research and its regulation by a plethora of mechanisms has been reported. Recently, genomic sequencing and functional genomic studies deepened our knowledge on the fundamental regulatory role of noncoding DNA. A large part of the genome is transcribed in an impressive number of noncoding RNAs. Among these, long noncoding RNAs (lncRNAs) have been reported to control several biological processes affecting gene expression at multiple levels from transcription to protein localization and stability. Up to now, more than 8000 lncRNAs were discovered as selectively expressed in cancer cells. Their elevated number and high expression specificity candidate these molecules as a valuable source of biomarkers and potential therapeutic targets. Rising evidence currently highlights a relevant function of lncRNAs on EMT regulation defining a new layer of involvement of these molecules in cancer biology. In this review we aim to summarize the findings on the role of lncRNAs on EMT regulation and to discuss their prospective potential value as biomarkers and therapeutic targets in cancer.

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“…Long noncoding RNAs (lncRNAs) are classified as transcribed RNA sequences >200 nucleotides and lack protein-coding capacity. 6 , 7 Long noncoding RNA functions as a key regulator in cell growth, 8 , 9 metastasis, 10 invasion, 11 and differentiation. 12 Moreover, lncRNAs also have key physiological effects on cancer progression.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: LncRNA MIR210HG Facilitates Non-Small Cell Lung Cancer Progression Through Directly Regulation of miR-874/STAT3 Axis

Zhang

Tian

et al. 2020

Dose-Response

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Background: Long noncoding RNAs are involved in the progression of multiple cancers. However, the expression and mechanism of microRNA (miR)210HG in non-small cell lung cancer (NSCLC) remain unclear. Methods: The levels of miR210HG and miR-874 were measured by quantitative real-time polymerase chain reaction in NSCLC tissue samples and cells. Non-small cell lung cancer cell proliferation, migration, and invasion were measured by Cell Counting Kit-8 and transwell assays. Luciferase analysis confirmed the interaction between miR210HG and miR-874. Results: Here, our data showed that miR210HG was overexpressed in NSCLC tissue samples and cells. In vitro functional assays showed that silencing miR210HG blocked NSCLC cell proliferation, migration, and invasion while promoting NSCLC cell radiosensitivity and chemoresistance. Mechanistically, miR-874 was directly regulated by miR210HG. Furthermore, miR-874 expression was reduced in NSCLC tissues and cells. The miR-874 mimic could mitigate the promoting effect of miR210HG on NSCLC cell progression. The data also showed that miR210HG promoted NSCLC cell progression through miR-181a expression by targeting STAT3. Conclusions: Our observations suggest that miR210HG is associated with NSCLC cell progression by regulating the miR-874/STAT3 axis.

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LncRNA TUSC7 suppresses pancreatic carcinoma progression by modulating miR‐371a‐5p expression

Cited by 24 publications

References 33 publications

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

Long Noncoding RNA and Epithelial Mesenchymal Transition in Cancer

RETRACTED: LncRNA MIR210HG Facilitates Non-Small Cell Lung Cancer Progression Through Directly Regulation of miR-874/STAT3 Axis

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