MiR‐155 targets TP53INP1 to regulate liver cancer stem cell acquisition and self‐renewal

Liu, Fengchao; Kong, Xin; Lv, Lin; Gao, Jian

doi:10.1016/j.febslet.2015.01.009

Cited by 52 publications

(41 citation statements)

References 35 publications

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“…Studies have shown that miR-155 is up-regulated in tumors and down-regulation of miR-155 can inhibit the formation of CSCs. Because TP53IPN1 is a tumor suppressor gene that regulates the cell cycle and induces apoptosis, miR-155, which targets the TP53INP1 gene, boosts the proliferation and self-renewal capacity of HCSCs [36]. FXR plays an important role in liver regeneration and helps prevent the development of liver cancer in addition to inhibiting the proliferation of HCSCs.…”

Section: The Function Of Micrornas In Carcinogenesis Of Hcscsmentioning

confidence: 99%

Characterization of the Role of MicroRNAs in Hepatic Cancer Stem Cells

Daia¹,

Zhang²

2017

Chemotherapy (Los Angel)

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Liver cancer is one of the most malignant tumors and is prone to relapse, metastasis and drug resistance. These phenomena can be explained by the existence of cancer stem cells (CSCs). CSCs have a strong ability to proliferate, are highly carcinogenic, exhibit multi-directional differentiation, develop drug resistance, and play critical roles in tumor radiotherapy, chemotherapy and tumor recurrence. miRNAs exert effects on oncogenes and tumor suppressor genes. There are distinctive miRNA expression profiles in different types of tumors, and these profiles are closely related to tumorigenesis, differentiation, metastasis and prognosis. Studies have shown that miRNAs are abnormally expressed in hepatocellular carcinoma and have important regulatory effects on the self-renewal and differentiation of hepatic cancer stem cells (HCSCs) as well as on the initiation of tumorigenesis. Therefore, it is critical to understand the impact of miRNAs in HCSC and the associated molecular mechanisms to develop new methods for the clinical diagnosis and treatment of liver cancer.

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Section: The Function Of Micrornas In Carcinogenesis Of Hcscsmentioning

confidence: 99%

Characterization of the Role of MicroRNAs in Hepatic Cancer Stem Cells

Daia¹,

Zhang²

2017

Chemotherapy (Los Angel)

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“…MiR-155 is overexpressed in different types of tumors, including colon cancer [16] and high expression of miR-155 correlates with poor prognosis in colorectal cancer patients [17] suggesting a pro-carcinogeneic role of miR-155. Increased RNA translation induced by miRNAs has been shown to be mediated via AU-rich elements (AREs) in the 3′ untranslated region (UTR) of mRNA for instance AUUA and AUUUA, as well as adjoining non-AU sequences [18] Notably, investigations have reported that miR-155 can regulate migration and invasion of certain tumor cell types, such as breast, pancreatic, hepatocellular and nasopharyngeal cancers [19–22]. However, the role and mechanism of MiR-155 in regulating chemokine-induced colon cancer cell migration is not known.…”

Section: Introductionmentioning

confidence: 99%

MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA

2017

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Colorectal cancer is the second most common cause of cancer-related death, which is due to migration of tumor cells to distant sites of metastasis. Accumulating data indicate that mciroRNAs play an important role in several aspects of colon cancer cell biology. Herein, we examined the role of miR-155-5p in colon cancer cell migration induced by the CCL17-CCR4 axis in HT-29 colon cancer cells. We found that miR-155-5p knockdown in serum starved colon cancer cells decreased CCL17-induced cell chemotaxis. Moreover, knocking down miR-155-5p markedly decreased CCL17-provoked activation of RhoA in colon cancer cells. Bioinformatics analysis predicted two putative binding sites in the AU-rich element at the 3′-UTR of RhoA mRNA. MiR-155-5p binding to RhoA mRNA was verified using a target site blocker and functionally validated by RNA immunoprecipitation assays, showing that miR-155-5p-dependent regulation of RhoA mRNA is mediated by AU-rich elements present in the 3′-UTR region. Taken together, these results show that miR-155-5p positively regulates RhoA mRNA levels and translation as well as cell migration in serum starved colon cancer cells and indicate that targeting miR-155-5p might be a useful strategy to antagonize colon cancer metastasis.

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“…Previous studies from our laboratory demonstrated that SFM enriches CSCs by promoting tumor sphere formation. 20 We cultured MHCC-97H and SMMC-7721 cells in SFM to investigate whether SPARC is associated with the CSC phenotype. Sphere formation was observed under an inverted microscope after 2 weeks (Fig.…”

Section: Resultsmentioning

confidence: 99%

Secreted protein acidic and rich in cysteine promotes epithelial–mesenchymal transition of hepatocellular carcinoma cells and acquisition of cancerstem cell phenotypes

Jiang

Liu

Wang

2019

J of Gastro and Hepatol

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Background and Aim Secreted protein acidic and rich in cysteine (SPARC) is a matricellular glycoprotein that plays a significant role in tumor development. SPARC has been indicated that promotes tumorigenesis, metastasis, and poor prognosis in prostate cancer and lung cancer. Therefore, we sought to investigate the molecular mechanisms of SPARC in regulating hepatocellular carcinoma (HCC). Methods We used spheroids cultured in serum‐free culture medium to obtain liver cancer stem cells. Flow cytometric analysis was performed to investigate percentage of CD133+ cells in liver cancer cells. Real‐time polymerase chain reaction and western blot were used to assess gene expression in cell lines. Transwell and wound healing assays were performed to indicate cell migration of HCC. Results Secreted protein acidic and rich in cysteine was upregulated in spheres formation in HCC cells. Overexpression of SPARC enhanced the ability to form tumor spheres and increased CD133 and Oct4 expressions. Besides, SPARC promoted the migration and epithelial–mesenchymal transition in HCC cells. Importantly, SPARC overexpression stimulated the formation of subcutaneous tumors in nude mice. Conclusions Our findings suggest that SPARC overexpression promotes tumor growth, inducing epithelial–mesenchymal transition and acquisition of a stem cell phenotype. What is more, research elucidating the biological mechanisms of SPARC may be beneficial to liver cancer treatment.

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MiR‐155 targets TP53INP1 to regulate liver cancer stem cell acquisition and self‐renewal

Cited by 52 publications

References 35 publications

Characterization of the Role of MicroRNAs in Hepatic Cancer Stem Cells

Characterization of the Role of MicroRNAs in Hepatic Cancer Stem Cells

MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA

Secreted protein acidic and rich in cysteine promotes epithelial–mesenchymal transition of hepatocellular carcinoma cells and acquisition of cancerstem cell phenotypes

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