We are analyzing https://link.springer.com/article/10.1007/s11010-014-1976-8.

Title:
miR-21 modulates chemosensitivity of tongue squamous cell carcinoma cells to cisplatin by targeting PDCD4 | Molecular and Cellular Biochemistry
Description:
Chemoresistance is a challenge for clinician in management of tongue cancer. Therefore, it is necessary to explore alternative therapeutic methods to overcome drug resistance. miRNAs are endogenous −22nt RNAs that play important regulatory roles by targeting mRNAs. miR-21, an essential oncogenic molecule, is associated with chemosensitivity of several human cancer cells to anticancer agents. In this study, we investigated the effects and molecular mechanisms of miR-21 in chemosensitivity of tongue squamous cell carcinoma cells (TSCC) to cisplatin. miR-21 expression was detected in tongue cancer tissue using RT-PCR and PDCD4 protein expression was measured using immunohistochemistry. miR-21 and(or) PDCD4 depleted cell lines were generated using miR-21 inhibitor and(or) siRNA. The viabilities of treated cells were analyzed using MTT assay. RT-PCR was used to detect miR-21 expression and immunoblotting was used to detect protein levels. Cell cycle and apoptosis were analyzed using propidium iodide (PI) staining and Annexin V/PI staining, respectively. The expression of miR-21 in tumorous tissue was significantly higher compared with adjacent normal tissue and loss of PDCD4 expression was observed in TSCCs. Transfection of miR-21 inhibitor induced sensitivity of TSCC cells (Tca8113 and CAL-27) to cisplatin. TSCC cells transfected with PDCD4 siRNA became more resistant to cisplatin therapy. We found an increase PDCD4 protein level following the transfection of miR-21 inhibitor using Western blot analysis. In addition, the enhanced growth-inhibitory effect by miR-21 inhibitor was weakened after the addition of PDCD4 siRNA. Suppression of miR-21 or PDCD4 could significantly promote or reduce cisplatin-induced apoptosis, respectively. Our data suggest that miR-21 could modulate chemosensitivity of TSCC cells to cisplatin by targeting PDCD4, and miR-21 may serve as a potential target for TSCC therapy.
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Keywords {🔍}

pubmed, article, google, scholar, cancer, cas, cell, cells, zhang, pdcd, central, carcinoma, microrna, squamous, cisplatin, wang, tongue, human, resistance, expression, tumor, chemosensitivity, oral, chen, inhibitor, apoptosis, access, biol, death, xian, privacy, cookies, content, data, research, gao, tscc, protein, chemotherapy, regulates, micrornas, gene, mol, programmed, suppressor, information, publish, search, molecular, targeting,

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         description: Chemoresistance is a challenge for clinician in management of tongue cancer. Therefore, it is necessary to explore alternative therapeutic methods to overcome drug resistance. miRNAs are endogenous −22nt RNAs that play important regulatory roles by targeting mRNAs. miR-21, an essential oncogenic molecule, is associated with chemosensitivity of several human cancer cells to anticancer agents. In this study, we investigated the effects and molecular mechanisms of miR-21 in chemosensitivity of tongue squamous cell carcinoma cells (TSCC) to cisplatin. miR-21 expression was detected in tongue cancer tissue using RT-PCR and PDCD4 protein expression was measured using immunohistochemistry. miR-21 and(or) PDCD4 depleted cell lines were generated using miR-21 inhibitor and(or) siRNA. The viabilities of treated cells were analyzed using MTT assay. RT-PCR was used to detect miR-21 expression and immunoblotting was used to detect protein levels. Cell cycle and apoptosis were analyzed using propidium iodide (PI) staining and Annexin V/PI staining, respectively. The expression of miR-21 in tumorous tissue was significantly higher compared with adjacent normal tissue and loss of PDCD4 expression was observed in TSCCs. Transfection of miR-21 inhibitor induced sensitivity of TSCC cells (Tca8113 and CAL-27) to cisplatin. TSCC cells transfected with PDCD4 siRNA became more resistant to cisplatin therapy. We found an increase PDCD4 protein level following the transfection of miR-21 inhibitor using Western blot analysis. In addition, the enhanced growth-inhibitory effect by miR-21 inhibitor was weakened after the addition of PDCD4 siRNA. Suppression of miR-21 or PDCD4 could significantly promote or reduce cisplatin-induced apoptosis, respectively. Our data suggest that miR-21 could modulate chemosensitivity of TSCC cells to cisplatin by targeting PDCD4, and miR-21 may serve as a potential target for TSCC therapy.
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      name:Department of Oral and Maxillofacial Surgery/Head and Neck Surgery, Stomatological Hospital, College of Stomatology, Xi’an Jiaotong University, Xi’an, China
      name:Department of Oral and Maxillofacial Surgery/Head and Neck Surgery, Stomatological Hospital, College of Stomatology, Xi’an Jiaotong University, Xi’an, China
      name:Department of Oral and Maxillofacial Surgery/Head and Neck Surgery, Stomatological Hospital, College of Stomatology, Xi’an Jiaotong University, Xi’an, China
      name:Department of Genetics and Molecular Biology, College of Medicine, Xi’an Jiaotong University, Xi’an, China
      name:Department of Oral and Maxillofacial Surgery/Head and Neck Surgery, Stomatological Hospital, College of Stomatology, Xi’an Jiaotong University, Xi’an, China
      name:Department of Oral and Maxillofacial Surgery/Head and Neck Surgery, Stomatological Hospital, College of Stomatology, Xi’an Jiaotong University, Xi’an, China
      name:Department of Oral and Maxillofacial Surgery, Stomatological Hospital, College of Stomatology, Xi’an Jiaotong University, Xi’an, China
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