miR-613 inhibits liver cancer stem cell expansion by regulating SOX9 pathway

Li, Bao; Liú, Dan; Yang, Pinghua; Li, Hengyu; Wang, Deyuan

doi:10.1016/j.gene.2019.05.015

Cited by 31 publications

(18 citation statements)

References 39 publications

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“…15 It was also reported that downregulation of miR-613 facilitated liver cancer stem cells, indicating that miR-613 was involved in tumor stemness. 16 Moreover, miR-613 suppressed migration and invasion in TNBC via targeting Daam1/RhoA signaling. 17 However, its function and mechanism in TNBC remain unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-613 Suppresses Chemoresistance and Stemness in Triple-Negative Breast Cancer by Targeting FAM83A</p>

Liu

Jiang

Han

2020

CMAR

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Section: Introductionmentioning

confidence: 99%

<p>miR-613 Suppresses Chemoresistance and Stemness in Triple-Negative Breast Cancer by Targeting FAM83A</p>

Liu

Jiang

Han

2020

CMAR

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“…In the past several decades, emerging evidence indicates that CSC is considered to have the ability to retain stem cell-like properties through self-renewal and differentiation and be responsible for tumor initiation, propagation, recurrence and resistance to therapy [14,39]. Moreover, CSC has now been suggested to bear a distinct metabolic phenotype and targeting CSC metabolism may provide a selective advantage to eventually take over and drive relapse of cancers [39,40]. Increasing evidence has indicated the existence of CSCs in OS [29,41] and yet, the mechanism of these CSCs in the progression of OS remains vague.…”

Section: Discussionmentioning

confidence: 99%

Untargeted LC–MS/MS analysis reveals metabolomics feature of osteosarcoma stem cell response to methotrexate

et al. 2020

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Background: Cancer stem cell (CSC) is identified in osteosarcoma (OS) and considered resistant to chemotherapeutic agents. However, the mechanism of osteosarcoma stem cell (OSC) resistant to chemotherapy remains debatable and vague, and the metabolomics feature of OSC is not clarified. Materials and methods: OSC was isolated by using sphere forming assay and identified. Untargeted LC-MS/MS analysis was performed to reveal the metabolomics feature of OSC and underlying mechanisms of OSC resistant to methotrexate (MTX). Results: OSC was efficiently isolated and identified from human OS 143B and MG63 cell lines with enhanced chemoresistance to MTX. The untargeted LC-MS analysis revealed that OSC showed differential metabolites and perturbed signaling pathways, mainly involved in metabolisms of fatty acid, amino acid, carbohydrate metabolism and nucleic acid. After treated with MTX, metabolomics feature of OSC was mainly involved metabolisms of amino acid, fatty acid, energy and nucleic acid. Moreover, compared with their parental OS cells response to MTX, the differential metabolites and perturbed signaling pathways were mainly involved in metabolism of amino acid, fatty acid and nucleic acid. What's more, Rap1 signaling pathway and Ras signaling pathway were involved in OS cells and their SCs response to MTX. Conclusion: Sphere-forming assay was able to efficiently isolate OSC from human OS cell lines and the untargeted LC-MS/MS analysis was suggested a sufficient methodology to investigate metabolomics features of OS cells and OSCs. Moreover, the metabolomics features of OSCs response to MTX might reveal a further understanding of chemotherapeutic resistance in OS.

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“…Meanwhile, other studies have shown that some miRNAs are associated with the regulation of cancer stem cells. For example, miR-613 inhibits liver CSC expansion by regulating the SOX9 pathway [16]. Our previous study also showed that multiple miRNAs, including let-7c, miR-200b, miR424 and miR-222, are essential to maintaining stem cell-like properties by regulating PBX3 [17].…”

Section: Introductionmentioning

confidence: 92%

Inhibiting CBX4 efficiently suppress YAP nucleus translocation in hepatocellular carcinoma cells to protect against sorafenib resistance

Zhao

Tian

et al. 2020

Preprint

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Background The discovery of biomarkers that predict the response to sorafenib and increase the efficiency of drug therapy represents a clinical challenge. This study aimed to investigate the possible role of inhibiting CBX4 to deregulate of CSCs and to evaluate the contribution of these molecules to sorafenib resistance in advanced HCC. Methods HCC cell lines and a xenograft mouse model with resistance to sorafenib were employed to analyze the effects of miR424 on CSC characteristics. RNA expression was analyzed by RT-PCR and next-generation sequencing in a cohort of 106 HCC cancer patients and sorafenib-resistant (SR) cell lines, respectively, to validate the key microRNAs and targets in the network. CBX4 expression was determined in HCC cells to examine YAP1-mediated stem-cell-like activation and its association with sorafenib resistance. Results MicroRNA and mRNA profiles of SR cell lines identified miR424 and its direct target CBX4 as significantly associated with stem-cell-like properties, poor survival and clinical characteristics. Functional experiments demonstrated that miR424 suppressed CBX4, and CBX4 induced nuclear translocation of YAP protein but was not associated with protein production. When YAP1 and CBX4 were modulated either alone or together in SR tumors with CA3 and UNC3866, respectively, tumorigenicity and stem-like properties were extremely inhibited, thus indicated that these compounds exerted a strong antitumor effect in vivo against SR HCC cells. Conclusions Our results revealed that blocking the crosstalk between CBX4 and YAP1 is critical in response to sorafenib resistance, and it could be a promising therapeutic strategy for patients with advanced HCC.

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miR-613 inhibits liver cancer stem cell expansion by regulating SOX9 pathway

Cited by 31 publications

References 39 publications

<p>miR-613 Suppresses Chemoresistance and Stemness in Triple-Negative Breast Cancer by Targeting FAM83A</p>

<p>miR-613 Suppresses Chemoresistance and Stemness in Triple-Negative Breast Cancer by Targeting FAM83A</p>

Untargeted LC–MS/MS analysis reveals metabolomics feature of osteosarcoma stem cell response to methotrexate

Inhibiting CBX4 efficiently suppress YAP nucleus translocation in hepatocellular carcinoma cells to protect against sorafenib resistance

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