miR-149 represses metastasis of hepatocellular carcinoma by targeting actin-regulatory proteins PPM1F

Luo, Gang; Chao, Ya-Ling; Tang, Bo; Li, Bosheng; Xiao, Yufeng; Xie, Rui; Wang, Shuming; Wu, Yingyi; Dong, Hui; Liu, Xiang-De; Yang, Shi‐Ming

doi:10.18632/oncotarget.5676

Cited by 69 publications

(64 citation statements)

References 35 publications

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“…Fan et al (25) also reported that miR-149 promoted cell proliferation and suppressed apoptosis by mediating JunB in T-cell acute lymphoblastic leukemia. In addition, Luo et al (26) indicated that miR-149 repressed the metastasis of hepatocellular carcinoma by targeting protein phosphatase 1F, an actin-regulatory protein. Despite the existence of numerous studies investigating miR-149 in several tumors, the biological function and molecular mechanism of miR-149 in ovarian cancer remain unclear to date.…”

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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“…For example, the overexpression of miR-149 suppressed the migration and invasion of HCC by targeting protein phosphatase, Mg 2+ /Mn 2+ dependent 1F directly (35). miR-148a induces hepatocytic differentiation by inhibiting the inhibitor of nuclear factor κα/NUMB/NOTCH pathway (36).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-33a downregulation is associated with tumorigenesis and poor prognosis in patients with hepatocellular carcinoma

Xie

Cong

Zhong³

et al. 2018

Oncol Lett

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Abstract. In order to examine the prognostic significance of miR-33a in patients with hepatocellular carcinoma (HCC), total RNA was extracted from 149 HCC biopsies, 36 of which were paired with para-carcinoma tissues, and miR-33a expression was measured by reverse transcription-quantitative polymerase chain reaction. The results demonstrated that miR-33a expression was decreased in HCC biopsies compared with normal liver tissue samples. It was also demonstrated that miR-33a expression was significantly associated with tumor foci number. Furthermore, overall and progression-free survival time was decreased in patients expressing low miR-33a with multiple tumor foci. Taken together, the low expression of miR-33a may be a potential risk factor for HCC. IntroductionHepatocellular carcinoma (HCC) is the sixth most prevalent cancer worldwide, and is associated with an extremely poor prognosis (1-3). A principal reason for the high mortality of this disease is the failure of early diagnosis for patients with HCC and the lack of effective therapies for patients with HCC in advanced stages. Despite a number of advances made in therapeutic strategies and surgery, the overall prognosis for patients with HCC remains poor due to the high rate of metastasis and recurrence (4-6). Hence, the characterization of the molecular mechanisms in HCC is urgently required to allow the development of novel treatment methods for patients with HCC.MicroRNAs (miRNAs/miRs) are small non-coding RNAs (21-23 nucleotides) that are transcribed as precursors in the nucleus and are subsequently processed into mature miRNAs in the cytoplasm. Mature miRNAs primarily function by sequence specific interactions with the 3'-untranslated regions of mRNAs, leading to the translational suppression or degradation of the mRNAs (7). An increasing number of studies have suggested that miRNAs serve an essential role as prognostic and predictive biomarkers in various types of cancer. For example, miR-1290 and miR-196b have been demonstrated to predict the chemotherapeutic response of patients with lung adenocarcinoma (8). miR-149, an anti-tumor miRNA, has been identified as dysregulated in a variety of types of cancer, including gastric (9), breast (10) and colorectal cancer (11,12).It is also reported that a number of are associated with HCC carcinogenesis, progression and metastasis, including miR-15b (13), miR-122 (14) and miR-29 (15). Furthermore, the low expression of miR-124 is significantly associated with a more aggressive phenotype and a poorer prognosis (16), whereas a high expression of miR-182 has been associated with intrahepatic metastasis and poor prognosis in HCC (17). However, the mechanism of these miRNAs and their regulatory networks in HCC remain elusive, and a number of miRNAs that are associated with HCC have yet to be considered.miR-33a was originally demonstrated to regulate lipid and cholesterol metabolism (18), and is an intronic miRNA located within the sequence of the sterol regulatory element binding protein 2 (SREBP-2) gene. miR-33a ...

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“…5A, B). Previous studies showed that PPM1F was a direct target of miR-149 in HCC [20]. We also identified PPM1F as a potential target of miR-149 based on its mirSVR score (−1.277) and PhastCons score (0.602) by using microRNA.org (http://www.microrna.org/).…”

Section: Silencing Snhg8 Counteracted the Tumor-promoting Effects Of mentioning

confidence: 99%

“…Previously, miR-149 has been demonstrated to function as a tumor suppressor in multiple malignant tumors [20,[28][29][30]. It suppresses cell proliferation and invasion by targeting FOXM1 in CRC [28], GIT1 in breast cancer [29], and ZBTB2 in GC [30].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

lncRNA SNHG8 Promotes the Tumorigenesis and Metastasis by Sponging miR-149-5p and Predicts Tumor Recurrence in Hepatocellular Carcinoma

Dong

Teng

Guo

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) are aberrantly expressed in multiple malignant tumors involved in tumor growth and metastasis. Accumulating data show that small nucleolar RNA host gene (SNHG) 1/12/20 plays a key role in the progression of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which SNHG8 contributes to HCC remain elusive and merit exploration. Methods: The association between SNHG8 expression and the clinicopathological characteristics and prognoses in HCC patients was analysed by using qRT-PCR analysis and the data from The Cancer Genome Atlas. Cell growth and metastatic potential were determined by MTT, colony formation, Transwell assays, and the mouse xenograft tumor model and lung metastasis model. Epithelial–mesenchymal transition markers were detected by western blot analysis. The binding capacity of SNHG8 with miRNAs was evidenced by bioinformatic analysis and a luciferase reporter assay. In addition, the rescue experiments were performed based on co-transfection with sh-SNHG8 and a miR-149 inhibitor in HCC cells. Results: The expression levels of lncRNA SNHG8 were dramatically increased in HCC tissues and cell lines as compared with the adjacent normal tissues, and SNHG8 expression was an independent prognostic factor of tumor recurrence in HCC patients. Furthermore, knockdown of SNHG8 inhibited cell proliferation, invasion, and lung metastasis in vitro and in vivo, whereas overexpression of SNHG8 reversed these effects. SNHG8 acted as a sponge of miR-149 and counteracted the tumor suppressive effects of mi R-149 in HCC cells. Expression of phosphatase, Mg2+/Mn2+ dependent 1F, a target of R-149, displayed a negative correlation with miR-149 expression but a positive correlation with SNHG8 expression in HCC specimens. Conclusion: As lncRNA SNHG8 may promote HCC tumorigenesis and metastasis by sponging miR-149, it is a potential candidate marker and therapeutic target for HCC.

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miR-149 represses metastasis of hepatocellular carcinoma by targeting actin-regulatory proteins PPM1F

Cited by 69 publications

References 35 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

MicroRNA-33a downregulation is associated with tumorigenesis and poor prognosis in patients with hepatocellular carcinoma

lncRNA SNHG8 Promotes the Tumorigenesis and Metastasis by Sponging miR-149-5p and Predicts Tumor Recurrence in Hepatocellular Carcinoma

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