[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China. *Corresponding author, E-mail:

Published: December 2017

Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.

Download full-text PDF

Source

Publication Analysis

Top Keywords

nci-h1975 cells
16
autophagy initiation
8
initiation stage
8
apoptosis nci-h1975
8
cpt treatment
8
nci-h1975
5
cells
5
cpt
5
[inhibition autophagy
4
stage enhances
4

Similar Publications

Coccinic acid exhibits anti-tumor efficacy against NSCLC harboring EGFR L858R/T790M mutation via the EGFR/STAT3 pathway.

Bioorg Chem

January 2025

Key Laboratory of Pu-er Tea Science, Ministry of Education, Yunnan Agricultural University, Kunming 650201, China; College of Science, Yunnan Agricultural University, Kunming 650201, China. Electronic address:

Epidermal growth factor receptor (EGFR) is a starring target for the treatment of non-small cell lung cancer (NSCLC). EGFR tyrosine kinase inhibitors (EGFR-TKIs) have been used to treat NSCLC patients with EGFR-activating mutations. However, most patients invariably develop resistance to these agents due to the occurrence of novel mutations at the EGFR kinase domain.

View Article and Find Full Text PDF

To overcome T790M mutation, a novel series of 4-indazolypyrimidine derivatives were developed as novel EGFR inhibitors employing a scaffold hopping drug design strategy. The biological activities of the target compounds were evaluated against two tumor cell lines (A431 and NCI-H1975), normal cell 2BS and EGFR kinase. The results indicated that the majority of the compounds exhibited promising antitumor activity and low toxicity.

View Article and Find Full Text PDF

The Effects of Nebivolol-Gefitinib-Loratadine Against Lung Cancer Cell Lines.

In Vivo

October 2024

Departamento de Farmacología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (Cinvestav-IPN), Ciudad de México, México;

Article Synopsis
  • * This study tested the combination of the antihistamine loratadine, beta-blocker nebivolol, and tyrosine-kinase inhibitor gefitinib on NSCLC cell lines A-549 and NCI-H1975, observing significant anti-cancer effects.
  • * The combination therapy effectively inhibited cell growth and increased apoptosis in both NSCLC cell lines, suggesting that this trio of drugs could be a promising alternative for treating lung cancer.
View Article and Find Full Text PDF

Cytochalasin H enhances sensitivity to gefitinib in non-small-cell lung cancer cells through inhibiting EGFR activation and PD-L1 expression.

Sci Rep

October 2024

Collaborative Innovation Center for Antitumor Active Substance Research and Development, Institute of Biochemistry and Molecular Biology, Guangdong Medical University, Zhanjiang, 524023, People's Republic of China.

In our previous study, we have isolated cytochalasin H (CyH) from endophytic fungus derived from mangrove plant and found that CyH inhibited the proliferation of non-small cell lung cancer (NSCLC) cells. Recently, epidermal growth factor receptor (EGFR) activation and programmed cell death 1 ligand (PD-L1) expression have been demonstrated to mediate NSCLC resistance to gefitinib, first-generation EGFR tyrosine kinase inhibitor (EGFR-TKI). Here, we further investigated the effect of CyH on EGFR activation, PD-L1 expression, and gefitinib sensitivity in NSCLC cell lines, A549 (wild-type EGFR), HCC827 (EGFR mutation), and NCI-H1975 (dual EGFR mutations and acquired gefitinib resistance) and animal model.

View Article and Find Full Text PDF

3D cultivation of non-small-cell lung cancer cell lines using four different methods.

J Cancer Res Clin Oncol

October 2024

Department of Clinical Sciences Lund, Division of Pathology, Lund University, BMC B13, Klinikgatan 26, Lund, SE-221 00, Sweden.

Purpose: The aim of this study was to set up reliable and reproducible culture conditions for 3D tumoroids derived from non-small cell lung cancer (NSCLC) cell lines to enable greater opportunity for successful cultivation of patient-derived samples.

Methods: Four NSCLC cell lines, two adenocarcinomas (A549, NCI-H1975) and two squamous cell carcinomas (HCC-95, HCC-1588), were first cultured in traditional 2D settings. Their expected expression profiles concerning TTF-1, CK7, CK5, and p40 status were confirmed by immunohistochemistry (IHC) before the generation of 3D cultures.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!