About: Gefitinib sensitization of cisplatin-resistant wild-type EGFR non-small cell lung cancer cells

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About: Gefitinib sensitization of cisplatin-resistant wild-type EGFR non-small cell lung cancer cells Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Gefitinib sensitization of cisplatin-resistant wild-type EGFR non-small cell lung cancer cells
Creator	Liu, · Cao, Weiya Li, Amin Liu, Jiachang Ma, Yongfang Tang, · Wang, Ruikai Xu, Ruyue Zhang, Rongbo Zhang, Yinci Zhou, Shuping
Source	Medline; PMC
abstract	PURPOSE: The usual first-line strategy of wild-type EGFR (wtEGFR) non-small cell lung cancer (NSCLC) remains cisplatin-based chemotherapy. However, cisplatin often loses effectiveness because most tumors acquire drug resistance over time. As EGFR is the most important pro-survival/proliferation signal receptor in NSCLC cells, we aimed at investigating whether cisplatin resistance is related to EGFR activation and further evaluating the combined effects of cisplatin/gefitinib (EGFR-tyrosine kinase inhibitor, EGFR-TKI) on cisplatin-resistant wtEGFR NSCLC cells. MATERIALS AND METHODS: EGFR activation was analysed in parental and cisplatin-resistant wtEGFR NSCLC cell lines (H358 and H358(R), A549 and A549(R)). Cellular proliferation and apoptosis of H358(R)/A549(R) cells treated with cisplatin or gefitinib, alone or in combination were investigated, and the related effector protein was detected by western blot analysis. Anti-tumor effect of two drugs combined was evaluated in animal models of H358(R) xenografts in vivo. RESULTS: EGFR was significantly phosphorylated in cisplatin-resistant wtEGFR NSCLC cells H358(R) and A549(R) than their parental cells. In H358(R) and A549(R) cells, anti-proliferative ability of gefitinib was further improved, and gefitinib combined with cisplatin enhanced inhibition of cellular survive/proliferation, and promotion of apoptosis in vitro. The combined effects were also associated with the inhibition of EGFR downstream effector proteins. Similarly, in vivo, gefitinib and cisplatin in combination significantly inhibited tumor growth of H358(R) xenografts. CONCLUSION: Abnormal activation of EGFR may induce wtEGFR NSCLC cell resistance to cisplatin. The combined effects of cisplatin/gefitinib suggest that gefitinib, as a combination therapy for patients with cisplatin-resistant wtEGFR NSCLC should be considered.
has issue date	2020-04-27(xsd:dateTime)
bibo:doi	10.1007/s00432-020-03228-4
bibo:pmid	32342201
has license	no-cc
sha1sum (hex)	7a77f5d9dfd36f52d244025b6c0878146ffaf3d4
schema:url	https://doi.org/10.1007/s00432-020-03228-4
resource representing a document's title	Gefitinib sensitization of cisplatin-resistant wild-type EGFR non-small cell lung cancer cells
has PubMed Central identifier	PMC7185832
has PubMed identifier	32342201
schema:publication	J Cancer Res Clin Oncol
resource representing a document's body	covid:7a77f5d9dfd36f52d244025b6c0878146ffaf3d4#body_text
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