miR-182 promotes tumor growth and increases chemoresistance&amp;nbsp;of human anaplastic thyroid cancer by targeting tripartite motif 8

Liu, Yao; Zhang, Bing; Shi, Tiefeng; Qin, Huadong

doi:10.2147/ott.s110468

Cited by 33 publications

(29 citation statements)

References 37 publications

(44 reference statements)

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“…Drug resistance is identified as a major obstacle in tumor chemotherapy, and miRNAs have been reported to serve critical roles in this process (17)(18)(19)(20)(21)(22)(23). To date, several studies have identified that miR-149 exerts a critical function in numerous types of tumors.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-149 suppresses the proliferation and increases the sensitivity of ovarian cancer cells to cisplatin by targeting X-linked inhibitor of apoptosis

et al. 2018

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Abstract. Currently, ovarian cancer is identified as one of the leading causes of cancer-associated mortality in females. Despite numerous efforts that were made on developing novel treatments for ovarian cancer, the survival rate remains unsatisfactory. Considering the important regulatory role of miRNAs in different types of cancer, the present study aims to identify a novel therapeutic target for treatment of ovarian cancer. The expression of miR-149 was detected using reverse transcription-quantitative polymerase chain reaction in cancerous and normal cells. Furthermore, the effects of miR-149 on ovarian cancer cell activities were investigated using MTT assay, colony formation, flow cytometry and western blotting analysis. In the present study, it was revealed that microRNA (miR)-149 was significantly downregulated in ovarian cancer tissues and cell lines, and that the miR-149 expression was correlated with the patient prognosis. In addition, it was observed that forced expression of miR-149 increased the sensitivity of ovarian cancer cell to cisplatin. Based on bioinformatics analysis and luciferase assay, X-linked inhibitor of apoptosis (XIAP) was identified as a direct target gene of miR-149 in ovarian cancer cells. It was also demonstrated that XIAP expression was upregulated in the ovarian cancer tissues and cell lines, while it was negatively correlated with miR-149 in these tissues and cells. Furthermore, results revealed that ectopic expression of XIAP was able to abolish the miR-149-enhanced cell sensitivity to cisplatin. In conclusion, the present study revealed that miR-149 functioned as a tumor suppressor in the progression of ovarian cancer, increasing the sensitivity of ovarian cancer cells to cisplatin treatment.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-149 suppresses the proliferation and increases the sensitivity of ovarian cancer cells to cisplatin by targeting X-linked inhibitor of apoptosis

et al. 2018

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“…Several studies have profiled differentially expressed miRNAs in lung cancer, among which miR‐182 was found to be upregulated more than six‐fold . miR‐182 was also demonstrated to contribute to chemoresistance to cisplatin in hepatocellular carcinoma, anaplastic thyroid cancer and colorectal cancer . In the present study, we study the possible role of miR‐182 in radioresistance in NSCLC, and our data show that miR‐182 could be a target for radiosensitization.…”

Section: Introductionmentioning

confidence: 53%

“…8 miR-182 was also demonstrated to contribute to chemoresistance to cisplatin in hepatocellular carcinoma, anaplastic thyroid cancer and colorectal cancer. [9][10][11] In the present study, we study the possible role of miR-182 in radioresistance in NSCLC, and our data show that miR-182 could be a target for radiosensitization.…”

mentioning

confidence: 70%

“…8,18 MiR-182 was also found to regulate cell proliferation, cancer metastasis, and chemoresistance to cisplatin. 10,18 A previous study also showed that knockdown of miR-182 inhibited lung cancer cell growth but enhanced cell invasion. In our study, by using a colony formation assay and apoptosis assay, we found that knockdown of miR-182 could enhance the radiosensitivity of lung cancer cells.…”

Section: Discussionmentioning

confidence: 96%

“…Several studies have revealed that miR‐182 is highly upregulated in lung cancers and lung cancer cells . MiR‐182 was also found to regulate cell proliferation, cancer metastasis, and chemoresistance to cisplatin . A previous study also showed that knockdown of miR‐182 inhibited lung cancer cell growth but enhanced cell invasion.…”

Section: Discussionmentioning

confidence: 97%

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MiR‐182 enhances radioresistance in non‐small cell lung cancer cells by regulating FOXO3

Chen

Dong

et al. 2019

Clin Exp Pharma Physio

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Summary Upregulated in lung cancer, miRNA‐182 was found to be related to cancer proliferation and chemoresistance. However, there is no report on the role of miR‐182 in radioresistance, which is a main obstacle of radiotherapy. In this study, we aim to depict the effect of miR‐182 inhibition on cellular sensitivity to ionizing radiation. Our data confirm that miR‐182 is upregulated in lung cancers and tissues and that miR‐182 is responsive to irradiation. We also show that miR‐182 knockdown suppresses cell proliferation and increases cell apoptosis after irradiation. DNA damage remains unrepaired in miR‐182 knockdown cells, which results in cell cycle arrest. Finally, we find that FOXO3 is a direct target of miR‐182 and that overexpression of FOXO3 enhances radiation resistance in miR‐182 knockdown cells. In conclusion, our data suggest that miR‐182 might account for radioresistance in lung cancer and that miR‐182‐FOXO3 provides a novel radiosensitizing target.

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Tripartite motif protein 25 is associated with epirubicin resistance in hepatocellular carcinoma cells via regulating PTEN/AKT pathway

Yuan¹,

Zheng²,

Tang³

2020

Cell Biology International

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Tripartite motif protein 25 (TRIM25) expression was altered in various human cancers. Herein, we found that the expression of TRIM25 was elevated in hepatocellular carcinoma (HCC) tissues and cell lines. Knockdown of TRIM25 increased the sensitivity of HCC HepG2 cells to epirubicin (EPI), as indicated by reduced cell viability, enhanced cell apoptosis, and downregulated P‐glycoprotein (P‐gp) and multiple drug‐resistance protein 1 (MRP1). Moreover, TRIM25 knockdown strengthened the effects of EPI on phosphatase and tensin homolog (PTEN) and phosphorylated (p)‐AKT. However, overexpression of TRIM25 exerted an opposite effect, weakening the sensitivity of Huh7 to EPI, and obviously increasing PTEN and reducing p‐AKT. Most important, all the changes induced by TRIM25 overexpression in Huh7 were reversed with additional treatment of LY294002 (an AKT pathway inhibitor). Notably, coimmunoprecipitation experiments confirmed the interaction between TRIM25 and PTEN. Knockdown of TRIM25 resulted in reduced ubiquitination of PTEN protein. Collectively, our data suggested that TRIM25 enhanced EPI resistance via modulating PTEN/AKT pathway, and targeting TRIM25 may enhance the sensitivity of HCC cells toward chemotherapy drugs.

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miR-182 promotes tumor growth and increases chemoresistance of human anaplastic thyroid cancer by targeting tripartite motif 8

Cited by 33 publications

References 37 publications

MicroRNA-149 suppresses the proliferation and increases the sensitivity of ovarian cancer cells to cisplatin by targeting X-linked inhibitor of apoptosis

MicroRNA-149 suppresses the proliferation and increases the sensitivity of ovarian cancer cells to cisplatin by targeting X-linked inhibitor of apoptosis

MiR‐182 enhances radioresistance in non‐small cell lung cancer cells by regulating FOXO3

Tripartite motif protein 25 is associated with epirubicin resistance in hepatocellular carcinoma cells via regulating PTEN/AKT pathway

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