miR‐383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1

Wan, Peiqi; Chi, Xiao-Jv; Du, Qiang; Luo, Jing; Cui, Xiao; Dong, Kun; Yan, Bing; Heres, Caroline; Geller, David A.

doi:10.1002/jcb.27286

Cited by 36 publications

(34 citation statements)

References 39 publications

(152 reference statements)

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“…26 Functionally, miR-383 serves as a tumor-suppressive miRNA in the abovementioned human cancer types. On the contrary, miR-383 is upregulated in cholangiocarcinoma 27 and stimulates cancer progression. To our knowledge, this study is the first to show that miR-383 expression is low in ESCC and that miR-383 directly targets SP1 mRNA in ESCC cells.…”

Section: Discussionmentioning

confidence: 99%

“…The latter was chosen for experimental verification because this miRNA has frequently been implicated in multiple types of human tumors. [23][24][25][26][27] The luciferase reporter assay was performed to test whether miR-383 can directly bind to FGD5-AS1 in ESCC cells. Either reporter plasmid FGD5-AS1-wt or FGD5-AS1-mut was transfected into TE-1 and Eca109 cells along with either agomir-383 or agomir-NC.…”

Section: Fgd5-as1 Interacts With Mir-383 and Sponges Mir-383 In Escc mentioning

confidence: 99%

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Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression

Jia

Zhang

Hong

et al. 2020

CMAR

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These authors contributed equally to this workPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms. Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment. Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown. Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383-SP1 axis, which may represent a novel target for ESCC therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Fgd5-as1 Interacts With Mir-383 and Sponges Mir-383 In Escc mentioning

confidence: 99%

Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression

Jia

Zhang

Hong

et al. 2020

CMAR

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“…In ccA, certain miRNAs have been previously demonstrated to exert stimulatory/suppressive effects on cancer progression (7). For example, miR-383 was found to act as a tumor suppressor in ccA and inhibits tumor development through decreasing the expression of interferon regulatory factor 1 (8). Through inhibiting aldolase A translation, miR-122-5p decreased bile duct carcinoma cell proliferation and promoted cell apoptosis (9).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑137 suppresses the proliferation, migration and invasion of cholangiocarcinoma cells by targeting WNT2B

et al. 2020

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It is widely known that abnormal regulation of microRNAs (miRNAs/miRs) may contribute to the occurrence or development of tumors. The objective of the present study was to elucidate the function and underlying mechanism of miR-137 in the progression of cholangiocarcinoma (ccA). The expression levels of miR-137 in ccA tissues and cell lines were measured using reverse transcription-quantitative PcR. The role of miR-137 in the proliferation of ccA cells was assessed using the cell counting Kit-8 assay, colony formation assay and cell cycle distribution analysis, while its effects on the migration and invasion of ccA cells were evaluated using Transwell assays. The function of miR-137 on ccA growth in vivo was also investigated using a xenograft mouse model. Furthermore, the association between miR-137 and Wnt family member 2B (WNT2B) was analyzed using bioinformatics, double luciferase assay and western blotting. It was verified that the expression of miR-137 was low in ccA tissues and cell lines, whereas increased expression of miR-137 significantly suppressed cell proliferation, decreased colony formation ability and induced G1 phase arrest. miR-137 overexpression suppressed the migration and invasion ability of TFK-1 and HuccT1 cells. Furthermore, the results of the xenograft mouse model assays revealed that miR-137 overexpression decreased tumor growth in vivo. The results of bioinformatics analysis and dual luciferase reporter assays demonstrated that WNT2B is directly regulated by miR-137. The expression of WNT2B and Wnt-pathway-related proteins was decreased when miR-137 was overexpressed. Restoring the expression of WNT2B notably reversed the inhibitory effect of miR-137 on CCA cells. Therefore, the findings of the present study demonstrated that miR-137 acts as a suppressor in ccA and inhibits ccA cell proliferation, migration and invasion through suppressing the expression of WNT2B.

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“…Using bioinformatics analysis and luciferase assay, we found that miR-216a-5p and miR-383-5p could directly regulate TIPRL expression through targeting the 3′-UTR of TIPRL. In recent years, accumulating evidence has demonstrated that miR-216a-5p and miR-383-5p are significantly elevated and function as oncogenic miRNAs in a variety of tumors ( 25 – 31 ). In particular, previous study have shown that miR-216a promotes invasion and metastasis in hepatocellular carcinoma through targeting TSLC1, PTEN, and SMAD7 ( 25 – 27 ), which is further confirmed in a variety of cell models ( 28 – 30 ).…”

Section: Discussionmentioning

confidence: 99%

“…In particular, previous study have shown that miR-216a promotes invasion and metastasis in hepatocellular carcinoma through targeting TSLC1, PTEN, and SMAD7 ( 25 – 27 ), which is further confirmed in a variety of cell models ( 28 – 30 ). Moreover, it has been reported that miR-383 promotes cholangiocarcinoma cell invasion and proliferation by suppressing IRF1 ( 31 ). More importantly, in gastric cancer, miR-216a is significantly upregulated ( 32 ), and elevation of miR-216a would favor a worse clinical outcome ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

TIPRL, a Novel Tumor Suppressor, Suppresses Cell Migration, and Invasion Through Regulating AMPK/mTOR Signaling Pathway in Gastric Cancer

Luan

Shi

et al. 2020

Front. Oncol.

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Invasion and metastasis of gastric cancer after curative resection remain the most common lethal outcomes. However, our current understanding of the molecular mechanism underlying gastric cancer metastasis is far from complete. Herein, we identified TOR signaling pathway regulator (TIPRL) as a novel metastasis suppressor in gastric cancer through genome-wide gene expression profiling analysis using mRNA microarray. Decreased TIPRL expression was detected in clinical gastric cancer specimens, and low TIPRL expression was correlated with more-advanced TNM stage, distant metastasis, and poor clinical outcome. Moreover, TIPRL was identified as a direct target of miR-216a-5p and miR-383-5p. Functional study revealed that re-expression of TIPRL in gastric cancer cell lines suppressed their migratory and invasive capacities, whereas inverse effects were observed in TIPRL-deficient models. Mechanistically, TIPRL downstream effectors and signaling pathways were investigated using mRNA microarray. Gene expression profiling revealed that TIPRL could not modulate the downstream genes at transcriptional levels, thereby implying that the regulation might occur at the post-transcriptional levels. We further demonstrated that TIPRL induced phosphorylation/activation of AMPK, which in turn attenuated phosphorylation of mTOR, p70S6K, and 4E-BP1, thereby leading to inactivation of mTOR signaling and subsequent suppression of cell migration/invasion in gastric cancer. Taken together, TIPRL acts as a novel metastasis suppressor in gastric cancer, at least in part, through regulating AMPK/mTOR signaling, likely representing a promising target for new therapies in gastric cancer.

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miR‐383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1

Cited by 36 publications

References 39 publications

<p>Long Noncoding RNA <em>FGD5-AS1</em> Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</p>

<p>Long Noncoding RNA <em>FGD5-AS1</em> Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</p>

MicroRNA‑137 suppresses the proliferation, migration and invasion of cholangiocarcinoma cells by targeting WNT2B

TIPRL, a Novel Tumor Suppressor, Suppresses Cell Migration, and Invasion Through Regulating AMPK/mTOR Signaling Pathway in Gastric Cancer

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