Evidence map›Paper›PMID 40156745›Full record

ArticleBulletin of experimental biology and medicine2025

Inhibition of Src Attenuates Stemness and Reverses Cisplatin Resistance of Non-Small-Cell Lung Cancer Cells.

A Li, R Wang

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Article in Bulletin of experimental biology and medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

A LiMedical School, Anhui University of Science & Technology, Huainan, China.
R WangPulmonary and Critical Care Medicine, First Affiliated Hospital, Anhui University of Science & Technology (Huainan First People's Hospital), Huainan, China. kerywang1984@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The first-line chemical drug cisplatin used to treat the non-small cell lung cancer (NSCLC) often becomes ineffective due to acquired drug resistance of cancer cells. This effect and related cancer progression are related to the presence of cancer stem cells in the tumor. Tyrosine kinase Src is responsible for the appearance and development of cancer stem cells. Here, we examined the effects of Src on the oncogenic properties of cisplatin-resistant NSCLC cell lines (H358R and A549R) and the effect of inhibition of this tyrosine kinase on the sensitivity of cancer cells to cisplatin by Western blotting and immunofluorescence staining as well as migration, invasion, sphere colony, and clone formation assays. In H358R and A549R cells, the levels of phosphorylated kinase Src (pSrc) and stemness marker CD133 were elevated in comparison with the parental ones. The cisplatin-resistant cells demonstrated increased self-renewal ability and formed significantly bigger tumor spheres than their parental cells. Inhibition of Src with its inhibitor CGP77675 attenuated stemness of H358R and A549R cells; moreover, it enhanced the inhibitory effects of cisplatin on cell proliferation, migration, and invasion. The data indicated that Src-induced stemness plays an important role in developed resistance of NSCLC cells to cisplatin. Inhibition of Src attenuated stemness and acquired resistance to cisplatin, which can be beneficial for treating the cisplatin-resistant NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungCisplatinDrug Resistance, NeoplasmLung NeoplasmsNeoplastic Stem Cellssrc-Family KinasesA549 CellsAC133 AntigenAntineoplastic AgentsCell Line, TumorCell MovementCell ProliferationHumansPhosphorylationAC133 AntigenAntineoplastic AgentsCisplatinsrc-Family Kinasescancer stemnesscisplatin resistancenon-small cell lung cancer (NSCLC)SrcSrc tyrosine kinase inhibitor CGP77675

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.