LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1

Chang, Zhiwei; Jia, Yong; Zhang, Weijie; Song, Lijie; Gao, Ming; Li, Mingjun; Zhao, Ruihua; Li, Jing; Ye, Zhong; Sun, Qiaozhi

doi:10.1186/s13046-018-0724-4

Cited by 90 publications

(67 citation statements)

References 32 publications

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“…In ESCC, several lncRNAs function as mediators of gene expression or signaling pathways that are involved in chemoresistance and radioresistance [5,20,38,127]. LINC00473, lncRNA FAM201A, and LINC00657 impair the effect of radiotherapy by acting as sponges for miRNAs [20,38,129].…”

Section: Non-coding Rnas Influence Chemoresistance and Radioresistancmentioning

confidence: 99%

Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

Feng

Zhang

Yao

et al. 2019

IJMS

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Esophageal squamous cell carcinoma (ESCC) is a highly prevalent tumor and is associated with ethnicity, genetics, and dietary intake. Non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs) have been reported as functional regulatory molecules involved in the development of many human cancers, including ESCC. Recently, several ncRNAs have been detected as oncogenes or tumor suppressors in ESCC progression. These ncRNAs influence the expression of specific genes or their associated signaling pathways. Moreover, interactions of ncRNAs are evident in ESCC, as miRNAs regulate the expression of lncRNAs, and further, lncRNAs and circRNAs function as miRNA sponges to compete with the endogenous RNAs. Here, we discuss and summarize the findings of recent investigations into the role of ncRNAs (miRNAs, lncRNAs, and circRNAs) in the development and progression of ESCC and how their interactions regulate ESCC development.

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Section: Non-coding Rnas Influence Chemoresistance and Radioresistancmentioning

confidence: 99%

Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

Feng

Zhang

Yao

et al. 2019

IJMS

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“…Accumulating evidences have shown that lncRNAs are closely associate with the occurrence and progression of malignancies and tumor drug resistance, which are served as tumor hallmarks. [11][12][13] For instance, lncRNA metastasis-associated lung adenocarcinoma transcript 1(MALAT1) has been reported to promote proliferation and metastasis in epithelial ovarian cancer, 14 hepatocellular carcinoma 15 and colorectal cancer. 16 Through literature review, we concluded that MALAT1 is involved in regulating proliferation, apoptosis, differentiation and metastasis of tumor cells.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway</p>

Dai¹,

Zhang²,

Li³

2020

CMAR

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Background: Many studies showed that long non-coding RNA MALAT1 is served as an oncogene. However, the specific role of MALAT1 in gastric cancer is not fully elucidated. The aim of this study is to elucidate the regulatory effects of MALAT1 on tumor development and cisplatin resistance in gastric cancer. Methods: TCGA database was applied to investigate the expression levels of MALAT1 in GC tissues and normal gastric tissues and its correlation with GC patients' survival. Univariate and multivariate analysis were performed to investigate whether MALAT1 expression is an independent risk for overall survival of gastric cancer patients. The expression of MALAT1 was detected by Quantitative real-time PCR. After knockdown or overexpression of MALAT1, the cellular functions of GC cells were detected by cell-proliferation, flow cytometry, transwell assay and colony formation assays, respectively. Western blot analysis was performed to detect the protein levels of Bcl-2 and key genes in the PI3K/AKT pathway in GC cells. Finally, CCK-8 assay was performed to explore the effect of MALAT1 on cisplatin resistance of GC cells. Results: Higher expression of MALAT1 was detected in GC tissues than that of adjacent normal tissues, high MALAT1 expression is an independent risk for overall survival of gastric cancer patients. Knockdown of MALAT1 inhibited proliferation, migration and invasion of GC cells, while overexpression of MALAT1 Overexpression of MALAT1 yielded opposite results. Western blot results showed that protein expressions of p-PI3K, p-AKT and p-STAT3 were downregulated after MALAT1 knockdown in GC cells, while these proteins were upregulated after MALAT1 overexpression. Additionally, the IC 50 in MGC803/CDDP cells transfected with si-MALAT1 was lower than in those transfected with si-NC. The apoptotic rate in MGC803 cells transfected with pcDNA-MALAT1 was remarkably lower than those transfected with NC. Conclusion: We demonstrated that MALAT1 is highly expressed in GC, high MALAT1 expression is an independent risk factor for OS among GC patients. Moreover, MALAT1 promotes malignant progression of GC and contributes to cisplatin resistance of GC cells, indicating MALAT1 may serve as a biological hallmark for predicting the prognosis of GC.

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“…Wang, Liu, et al, 2016). The previous study has verified (Chang et al, 2018). It is reported that TUSC7 inhibits temozolomide resistance by targeting miR-10a in glioblastoma and acts as a tumor suppressor in colorectal cancer (Ren et al, 2012;Shang, Tang, Pan, Hu, & Hong, 2018).…”

Section: Discussionmentioning

confidence: 82%

“…Evidence is increasing that TUSC7 is considered as a robust suppressor in diverse cancers (Y. Wang, Liu, et al, ). The previous study has verified lncRNA‐TUSC7/miR‐224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1 (Chang et al, ). It is reported that TUSC7 inhibits temozolomide resistance by targeting miR‐10a in glioblastoma and acts as a tumor suppressor in colorectal cancer (Ren et al, ; Shang, Tang, Pan, Hu, & Hong, ).…”

Section: Discussionmentioning

confidence: 92%

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

Yue

Guo

2019

Journal Cellular Physiology

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Pancreatic carcinoma is one of the most common and lethal human malignancies worldwide. Long noncoding RNAs (lncRNAs) are a well‐known type of nonprotein‐coding transcripts implicated in cancer development and progression. Increasing evidence has indicated that lncRNA tumor suppressor candidate 7 (TUSC7) is a novel cancer suppressor gene in various cancers. Nevertheless, the function of TUSC7 in pancreatic carcinoma is urgent to be clarified. We found that TUSC7 was notably decreased in tissues and cell lines of pancreatic carcinoma. Moreover, the low expression of TUSC7 was correlated with advanced clinical grades and poorer overall survival. Our findings revealed that TUSC7 repressed cell proliferation, migration, invasion, epithelial–mesenchymal transition, and stemness whereas facilitated cell apoptosis of pancreatic carcinoma cells. Further investigations demonstrated that miR‐371a‐5p directly bound with TUSC7 and negatively regulated by TUSC7. MiR‐371a‐5p rescued the inhibitory effects of TUSC7 on the development of pancreatic carcinoma. We conclude that lncRNA TUSC7 suppresses pancreatic carcinoma progression by modulating miR‐371a‐5p expression, indicating an innovative therapeutic strategy for pancreatic carcinoma.

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LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1

Cited by 90 publications

References 32 publications

Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

<p>LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway</p>

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

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