LncRNA MT1JP functions as a ceRNA in regulating FBXW7 through competitively binding to miR-92a-3p in gastric cancer

Zhang, Gang; Li, Shuwei; Lü, Jiafeng; Ge, Yuqiu; Wang, Qiaoyan; Ma, Gaoxiang; Zhao, Qinghong; Wu, Dongdong; Gong, Weida; Du, Mulong; Chu, Haiyan; Wang, Meilin; Zhang, Aihua; Zhang, Zhengdong

doi:10.1186/s12943-018-0829-6

Cited by 235 publications

(174 citation statements)

References 34 publications

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“…Previous references proved that MT1JP has been played a tumor suppressor gene in a lot of tumors (L. H. Liu, Yue, et al, 2016; Yang et al, ; G. Zhang et al, ; Zhu, Ma, et al, ). For instance, L. H. Liu, Yue, et al () first indicated that MT1JP expression was downregulated in the cancer tissues and downregulation expression of MT1JP promoted cancer cell deterioration and cancer formation through regulating p53 expression via interactions with the TIAR.…”

Section: Discussionmentioning

confidence: 99%

Retracted: LncRNA MT1JP functions as a tumor suppressor via regulating miR‐214‐3p expression in bladder cancer

Wang

Zhu

et al. 2019

Journal Cellular Physiology

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Growing evidence suggested that the long noncoding RNAs (lncRNAs) regulate several pathophysiological processes in tumorigenesis and may be new biomarkers for tumor therapy. In this study, we studied the expression and role of lncRNA MT1JP in the development of bladder cancer. We demonstrated that the expression of MT1JP was downregulated in bladder tumor samples and cell lines. Ectopic expression of MT1JP suppressed cell proliferation, cycle, and invasion in bladder cancer. In addition, our result suggested that miR‐214‐3p overexpression decreased the luciferase activity of wild‐type MT1JP but not mutated‐type MT1JP and elevated expression of MT1JP decreased miR‐214‐3p expression in the bladder cancer cell. Furthermore, we indicated that the expression of miR‐214‐3p was upregulated in bladder tumor samples and cell lines. Ectopic expression of miR‐214‐3p promoted cell proliferation, cycle, and invasion in bladder cancer. MT1JP suppressed cell proliferation, cycle, and invasion via negative modulation of miR‐214‐3p in bladder cancer. These data suggested that lncRNA MT1JP acts a tumor suppressor gene in bladder cancer progression, considering MT1JP as a new therapeutic target in bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Retracted: LncRNA MT1JP functions as a tumor suppressor via regulating miR‐214‐3p expression in bladder cancer

Wang

Zhu

et al. 2019

Journal Cellular Physiology

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“…As reported previously, lncRNAs can modulate gene expression in human cancers by acting as ceRNAs. [26][27][28][29][30] Here, we designed mechanism experiments to detect whether ARAP1-AS1 can act as a ceRNA in BCa. The localization of ARAP1-AS1 was detected in BCa cells.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ARAP1-AS1 promotes the progression of bladder cancer by regulating miR-4735-3p/NOTCH2 axis

Teng

Jia

et al. 2018

Cancer Biology & Therapy

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Accumulative reports have documented the critical functions of long non-coding RNAs (lncRNAs) in the progression of malignant tumors, including bladder cancer (BCa). LncRNA ARAP1-AS1 was chosen to be the object of this study due to it was significantly upregulated in the BCa samples of TCGA database. qRT-PCR further validated the dysregulation of ARAP1-AS1 in 88 pairs of BCa tissues and six BCa cells. Kaplan Meier analysis was utilized to analyze the prognostic value of ARAP1-AS1 for patients with BCa. To evaluate the oncogenic property of ARAP1-AS1 in bladder cancer, loss-of-function assays were conducted in two BCa cells in which ARAP1-AS1 was expressed highest. Mechanically, ARAP1-AS1 was enriched in the cytoplasm of BCa cells, suggesting that ARAP1-AS1 might act as a ceRNA to regulate gene expression and biological processes in bladder cancer. It was certified that ARAP1-AS1 can bind with miR-4735-3p in BCa cells. Moreover, functional assays supported the hypothesis that miR-4735-3p is a tumor suppressor in BCa. Additionally, NOTCH2 mRNA could be targeted by miR-4735-3p in BCa cells. The results of all mechanism experiments indicated that ARAP1-AS1 regulated miR-4735-3p/NOTCH2 axis in BCa by acting as a ceRNA. All our research findings may bring novel insights into the treatment of bladder cancer. ARTICLE HISTORY

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“…miRNAs and lncRNAs belong to noncoding RNAs and increasing evidence demonstrated that lncRNA can act as competing endogenous RNAs (ceRNAs) to regulate mRNA by binding their common miRNAs in various cancers. [17][18][19][20] These regulatory networks are widely involved in tumor occurrence, development, apoptosis, and drug resistance in GC. For instance, HOTAIR contributed to cisplatin resistance by regulating VEGFA and PIK3R2 via targeting miR-126 in GC.…”

Section: Introductionmentioning

confidence: 99%

<p>lncRNA MALAT1 modulates oxaliplatin resistance of gastric cancer via sponging miR-22-3p</p>

Zhang

2020

OTT

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Objective: Various regulatory mechanisms have been demonstrated to be associated with cancer progression. ncRNA and mRNA play important roles in gastric cancer (GC) cell growth and drug resistance, respectively. However, the regulatory network of ncRNA and mRNA in GC oxaliplatin (OXA) resistance has not been fully clarified. Methods: The expression of miR-22-3p, MALAT1, and zinc finger protein 91 (ZFP91) was detected in tissues and cells using quantitative real-time PCR. The protein level of ZFP91 was measured by Western blot analysis. Luciferase reporter, pull-down, and RNA immunoprecipitation assays were used to determine the relationship between MALAT1, miR-22-3p, and ZFP91. MTT assay was applied to measure cell survival and proliferation. Cell apoptosis was detected using flow cytometry. Tumor xenograft assay was used to detect the function of miR-22-3p in vivo. Results: In this study, we found that MALAT1 and ZFP91 expression was upregulated while the expression of miR-22-3p was downregulated in GC/OXA tissues and cells. Additionally, miR-22-3p was a target miRNA of MALAT1 and ZFP91 was a target mRNA of miR-22-3p. Functional studies showed that the knockdown of MALAT1 or overexpression of miR-22-3p inhibited GC/OXA cell survival, proliferation, and drug resistance as well as induced apoptosis, which could be reversed by the inhibition of miR-22-3p or overexpression of ZFP91. Conclusion: We observed a new regulatory network for MALAT1 in drug resistance of GC. MALAT1 modulates ZFP91 to promote GC cells OXA resistance via sponging miR-22-3p.

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LncRNA MT1JP functions as a ceRNA in regulating FBXW7 through competitively binding to miR-92a-3p in gastric cancer

Cited by 235 publications

References 34 publications

Retracted: LncRNA MT1JP functions as a tumor suppressor via regulating miR‐214‐3p expression in bladder cancer

Retracted: LncRNA MT1JP functions as a tumor suppressor via regulating miR‐214‐3p expression in bladder cancer

Long non-coding RNA ARAP1-AS1 promotes the progression of bladder cancer by regulating miR-4735-3p/NOTCH2 axis

<p>lncRNA MALAT1 modulates oxaliplatin resistance of gastric cancer via sponging miR-22-3p</p>

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