MiR-122 Reverses the Doxorubicin-Resistance in Hepatocellular Carcinoma Cells through Regulating the Tumor Metabolism

Pan, Chen‐Wei; Wang, Xiaodong; Shi, Ke‐Qing; Zheng, Yi; Li, Jie; Chen, Yongping; Jin, LJ; Pan, Zhenzhen

doi:10.1371/journal.pone.0152090

Cited by 68 publications

(61 citation statements)

References 37 publications

(37 reference statements)

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“…The tumor suppressor miR-122 has been found to promote adriamycin sensitivity in HCC cells through inhibiting cell cycle, anti-apoptotic effector factors and ABC transporters [82][83][84]. Similarly, miR-31 has been found to increase the sensitivity of HCC cells to adriamycin via silencing the expression of NDRG3 [85].…”

Section: Mirnas and Resistance To Adriamycinmentioning

confidence: 99%

The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma

et al. 2019

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Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and the second most lethal human cancer. A portion of patients with advanced HCC can significantly benefit from treatments with sorafenib, adriamycin, 5-fluorouracil and platinum drugs. However, most HCC patients eventually develop drug resistance, resulting in a poor prognosis. The mechanisms involved in HCC drug resistance are complex and inconclusive. Human transcripts without protein-coding potential are known as noncoding RNAs (ncRNAs), including microRNAs (miRNAs), small nucleolar RNAs (snoRNAs), long noncoding RNAs (lncRNAs) and circular RNA (circRNA). Accumulated evidences demonstrate that several deregulated miRNAs and lncRNAs are important regulators in the development of HCC drug resistance which elucidates their potential clinical implications. In this review, we summarized the detailed mechanisms by which miRNAs and lncRNAs affect HCC drug resistance. Multiple tumorspecific miRNAs and lncRNAs may serve as novel therapeutic targets and prognostic biomarkers for HCC.

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Section: Mirnas and Resistance To Adriamycinmentioning

confidence: 99%

The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma

et al. 2019

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“…The absence of miR-122 is found to enhance the proliferation, metastatic, and tumorigenic properties of cancer cells [34,35]. On the other hand, the recovery of miR-122 expression has been reported to increase the chemosensitivity of cancer cells [36,37]. The overexpression of miR-122 may represent a potential strategy for cancer treatments.…”

Section: Discussionmentioning

confidence: 99%

miR-122 Targets X-Linked Inhibitor of Apoptosis Protein to Sensitize Oxaliplatin-Resistant Colorectal Cancer Cells to Oxaliplatin-Mediated Cytotoxicity

Hua

Zhu²,

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Although oxaliplatin is one of the most effective chemotherapeutic drugs used to treat colorectal cancer (CRC), long-term administration usually induces acquired drug resistance during the course of treatment. Thus, there is an urgent need to explore novel strategies to improve the efficiency of cancer therapy. The aim of this study was to explore the effect of microRNA-122 (miR-122) on reversing oxaliplatin resistance in CRC. Methods: The expression of miR-122 in CRC cells was examined by quantitative reverse transcriptase real-time PCR. The cytotoxicity of oxaliplatin against CRC cells was evaluated by Cell Counting Kit-8 assays. Mitochondrial membrane potentials and cell apoptotic rates were measured by flow cytometry. Cellular protein expression and interactions were detected by western blot and co-immunoprecipitation. Results: Established oxaliplatin-resistant SW480 and HT29 cells (SW480/OR and HT29/OR) expressed significantly higher levels of X-linked inhibitor of apoptosis protein (XIAP) and lower levels of miR-122 compared with normal SW480 and HT29 cells, respectively. Our results showed that the downregulation of miR-122 was responsible for the overexpression of XIAP in these oxaliplatin-resistant CRC cells. We then found that the recovery of miR-122 expression can sensitize SW480/OR and HT29/OR cells to oxaliplatin-mediated apoptosis through the inhibition of XIAP expression. Conclusion: Upregulation of XIAP in CRC cells is responsible for the acquired resistance to oxaliplatin. Furthermore, miR-122 reversed oxaliplatin resistance in CRC by targeting XIAP.

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“…The metabolic changes in Huh7 cells may be a contributor to the discrepancies between the cell line and hepatocytes in vivo 46 . Since the ECM can alter metabolisms in carcinoma cells including the energy pathways 50 The ECM changes amino acids bioavailability in Huh7 cells Availability of amino acids, the building block of proteins, may also be affected by the ECM and the 3D culture.…”

Section: The Ecm Modulates Energy Metabolism In Huh7 Cells Toward Phymentioning

confidence: 99%

Microfibrous extracellular matrix enhances in vitro modeling of the liver hepatocytes by modulating metabolism and integrin expression

Huang¹,

Jones²,

Chung³

et al. 2020

Preprint

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MiR-122 Reverses the Doxorubicin-Resistance in Hepatocellular Carcinoma Cells through Regulating the Tumor Metabolism

Cited by 68 publications

References 37 publications

The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma

The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma

miR-122 Targets X-Linked Inhibitor of Apoptosis Protein to Sensitize Oxaliplatin-Resistant Colorectal Cancer Cells to Oxaliplatin-Mediated Cytotoxicity

Microfibrous extracellular matrix enhances in vitro modeling of the liver hepatocytes by modulating metabolism and integrin expression

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