Individualized treatment of NSCLC: From research to clinical practice

Y, Wang; Zd, Liu; Lm, Zhao; Cx, Du; Xm, Xi; Yl, Mi; Peng, Yingwei; Li, WG; Cheng, Fiona Tsui-Fen; Xr, Zhang; Yq, Zheng; Kk, Tang; Yang, Hongyan; Dt, Chu

doi:10.4149/neo_2013_070

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…International Publisher or drug resistance could be acquired after a period of chemotherapy, resulting in treatment failure and tumor recurrence. Therefore, understanding the mechanism of acquisition of cisplatin resistance in NSCLC cells would benefit patient in clinical settings [3].…”

Section: Ivyspringmentioning

confidence: 99%

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Nedaplatin reduces multidrug resistance of non-small cell lung cancer by downregulating the expression of long non-coding RNA MVIH

et al. 2020

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Cisplatin-based chemotherapy is the standard treatment for non-small cell lung cancer (NSCLC). However, drug resistance emergences after treatment. Long non-coding RNA microvascular invasion in hepatic cancer (MVIH) plays an important role in drug resistance in a variety of cancers. This study investigates the role of nedaplatin on multidrug resistance in NSCLC and its relationship with MVIH. Lung cancer A549 and H1650 cells were treated with cisplatin to obtain multidrug-resistant A549/DDP and H1650/ DDP cells. A549/DDP and H1650/ DDP cells were treated with nedaplatin, MVIH siRNA and siRNA NC. It was found that both MVIH siRNA and nedaplatin significantly reduce the mRNA expression of MVIH in A549/DDP and H1650/ DDP cells. MTT assay showed that the proliferation of MDR cells was significantly higher than that of other cells. Nedaplatin and MVIH siRNA significantly inhibit the proliferation of A549 and H1650 cells. The results of colony formation assay were consistence with MTT results. Nedaplatin and MVIH siRNA significantly reduced colony formation in MDR cells. Flow cytometry showed that NDP and MVIH siRNA significantly decrease the proportion of cells in G0/G1 and increase the proportion of cells in S phase compared with untreated and MDR cells. The apoptotic rate of MDR cells was significantly lower than that of other cells, while the apoptosis rate of cells in NDP and MVIH siRNA group was significantly higher than that of the other three groups of cells. Wound healing assay and Transwell chamber experiments confirmed that both NDP and MVIH siRNA significantly reduced the migration and invasion abilities of MDR cells. The expression of E-cadherin in MDR cells was significantly lower than that in untreated cells, and the expression of N-cad, α-SMA and Vimentin significantly increased in the MDR cells. NPD and MVIH siRNA reverse the EMT process. In conclusion, LncRNA MVIH is upregulated in drug resistant NSCLC cells. Nedaplatin can reduce the expression of MVIH and reverse EMT process, thus reversing the drug resistance of cisplatin in non-small cell lung cancer cells.

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Section: Ivyspringmentioning

confidence: 99%

“…Tumor size was measured every 3 days after one week post implantation. Mice were scarified when tumors reached a volume of maximal 5000 mm 3 .…”

Section: Animal Experimentsmentioning

confidence: 99%

Nedaplatin reduces multidrug resistance of non-small cell lung cancer by downregulating the expression of long non-coding RNA MVIH

et al. 2020

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“…This technology includes a sandwich nucleic acid hybridization method in which mRNAs are captured through cooperative hybridization of multiple probes and subsequently coupled with a fluorescence signal amplification system (17). The signals were detected by the Luminex 200 system, as described previously (17).…”

Section: Ercc1 Tubb3 Tyms Rrm1 and Egfr Mrna Expression Analysis mentioning

confidence: 99%

EGFR and K-RAS mutations and ERCC1, TUBB3, TYMS, RRM1 and EGFR mRNA expression in non-small cell lung cancer: Correlation with clinical response to gefitinib or chemotherapy

Guo

Zhang

et al. 2015

Molecular and Clinical Oncology

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Abstract. Personalizing medicines has refined the traditional treatments for non-small-cell lung cancer (NSCLC). In the present study, efforts towards personalizing delivery of care based on the status of EGFR and K-RAS mutations, and mRNA expression levels of ERCC1, TUBB3, TYMS, RRM1 and EGFR by choosing appropriate treatments for 52 patients with NSCLC were discussed. Among these 52 NSCLC patients, there were 14 patients treated with gefitinib. Ten patients with EGFR exon 21 point mutations or exon 19 deletions had better treatment outcomes following gefitinib treatment (71.4%). There were 38 patients treated with platinum-based chemotherapy. Docetaxel-platinum based chemotherapy was chosen as the first-line treatment when the patients had low or median ERCC1/TUBB3 expression and gemcitabine-platinum based chemotherapy was chosen when the patients had low or median ERCC1/RRM1 expression. In total, 26 cases had mRNA expression levels of ERCC1/TUBB3 or ERCC1/RRM1 that could be used to predict the treatment outcomes of chemotherapy (68.4%). The present results indicated that the mutation status of EGFR, as well as the mRNA expression levels of ERCC1, TUBB3 and RRM1, could be used as predictors of the response to gefitinib or chemotherapy. IntroductionLung cancer, of which nearly 80-85% is diagnosed as non-small-cell lung cancer (NSCLC), is one of the leading causes of fatality worldwide (1). The adjuvant chemotherapy, including the combinations of platinum and cytotoxic agents (such as docetaxel and gemcitabine) and epidermal growth factor receptor (EGFR)-targeted therapy, such as gefitinib (AstraZeneca, London, UK), has become common treatments for NSCLC (2). However, drug resistance causes unsatisfactory clinical responses to these medicines. Therefore, it is essential to understand the molecular markers associated with resistance to these medicines, to aid oncologists in choosing the more effective anti-tumor drugs for patients to achieve the most advantageous potential outcomes.The major molecular markers associated with clinical response to gefitinib or chemotherapy in NSCLC include the status of EGFR, K-RAS mutations and mRNA expression levels of excision repair cross-complementing 1 (ERCC1), class III β-tubulin (TUBB3), thymidylate synthase (TYMS), ribonucleotide reductase subunit M1 (RRM1) and EGFR (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). EGFR is a member of the ErbB family of receptors. Mutations within the tyrosine kinase domain of EGFR account for increased sensitivity to the tyrosine kinase inhibitor (TKIs), such as gefitinib (3,4). However, an insertion mutation and the point mutation T790M in exon 20 of EGFR are associated with resistance to TKIs (5). Previous studies have demonstrated that overexpression of EGFR was associated with increased sensitivity to gefitinib (6,7). K-RAS encodes a small guanosine triphosphate (GTP)-binding protein involved in numerous cellular processes, including proliferation and apoptosis (8). The wild-type K-RAS protein has intrinsic GTPase activity that catalyzes the...

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“…Several SNPs of genes encoding enzymes involved in different mechanisms of DNA repair, including nucleotide excision repair (NER): ERCC1, XPA, XPC, XPG, XPD, MMS18L, base excision repair (BER): XRCC1, BRCA1, mismatch repair (MMR): RECQ1 as well as nucleotide synthesis: RRM1, TS, MTHFR, have been investigated in patients with advanced NSCLC [8][9][10][11][12][13]. These SNPs, associated with lung cancer risk and response to treatment, may be also the predictors for toxicity of chemotherapy [14][15][16][17]. Unfortunately, only few clinical trials, that assess the association between SNPs of DNA repair genes and the toxicity of various chemotherapy regimens, are available in literature.…”

Section: Introductionmentioning

confidence: 98%

The relationship between polymorphisms of genes regulating DNA repair or cell division and the toxicity of platinum and vinorelbine chemotherapy in advanced NSCLC patients

et al. 2015

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Individualized treatment of NSCLC: From research to clinical practice

Cited by 5 publications

References 36 publications

Nedaplatin reduces multidrug resistance of non-small cell lung cancer by downregulating the expression of long non-coding RNA MVIH

Nedaplatin reduces multidrug resistance of non-small cell lung cancer by downregulating the expression of long non-coding RNA MVIH

EGFR and K-RAS mutations and ERCC1, TUBB3, TYMS, RRM1 and EGFR mRNA expression in non-small cell lung cancer: Correlation with clinical response to gefitinib or chemotherapy

The relationship between polymorphisms of genes regulating DNA repair or cell division and the toxicity of platinum and vinorelbine chemotherapy in advanced NSCLC patients

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