Fluorinated thiazolidinols cause cell death in A549 lung cancer cells via PI3K/AKT/mTOR and MAPK/ERK signalling pathways

Background: The World Health Organization (WHO) estimated that the number of cancer-related deaths was 9.6 million in 2018 and 2.09 million deaths occurred by lung cancer. The American Institute for Cancer Research (AICR) also observed gender preferences in lung cancer, common in men than women. Since the past decade, nanoparticles have now been widely documented for their anti-cancer properties, which signifies that the development of nanotechnology would be a future diagnosis and treatment strategy for lung cancer. Objective: The current study aimed to investigate the role of biosynthesized CdS nanoparticles (CdS NPs) in lung cancer cells (A549). Therefore, whether the CdS NP induces lung cancer cell death and the underlying mechanism is yet to be elucidated. Methods: Literature was searched from various archives of biomedical and life science journals. Then, CdS NPs were biosynthesized and characterized by traditional and cutting-edge protocols. The CdS NP-mediated cell death was elucidated following standard protocols. Results : CdS NPs induced cytotoxicity towards A549 cells in a dose-dependent manner. However, such a death mechanism does not go through necrosis. Intracellular reactive oxygen species (ROS) accumulation and mitochondrial membrane depolarization demonstrated that cell death is associated with intracellular ROS production. Furthermore, increased sub-G1 population, Bax expression, and decreased Bcl-2 expression revealed that the death was caused by apoptosis. Conclusion: CdS NPs promote apoptosis-mediated lung cancer cell death through ROS production.

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Discovery of 2′-hydroxychalcones as autophagy inducer in A549 lung cancer cells

Organic & Biomolecular Chemistry ◽

10.1039/c3ob42429d ◽

2014 ◽

Vol 12 (19) ◽

pp. 3062-3070 ◽

Cited By ~ 14

Author(s):

Fang-Wu Wang ◽

Sheng-Qing Wang ◽

Bao-Xiang Zhao ◽

Jun-Ying Miao

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Lung Cancer Cells ◽

Lung Cancer Cell ◽

A549 Lung Cancer Cell ◽

A549 Lung

A series of 2′-hydroxychalcone derivatives was synthesized and the effects of all the compounds on growth of A549 lung cancer cell were investigated.

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Modes of cell death induced by tetrahydroisoquinoline-based analogs in MDA-MB-231 breast and A549 lung cancer cell lines

Drug Design Development and Therapy ◽

10.2147/dddt.s152718 ◽

2018 ◽

Vol Volume 12 ◽

pp. 1881-1904 ◽

Cited By ~ 5

Author(s):

Marcel Nel ◽

Annie Joubert ◽

Wolfgang Dohle ◽

Barry Potter ◽

Anne Theron

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cell Lines ◽

Cancer Cell ◽

Cancer Cell Lines ◽

Lung Cancer Cell ◽

A549 Lung Cancer Cell ◽

A549 Lung

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Regulation of Bax-dependent apoptosis by mitochondrial deubiquitinase USP30

Cell Death Discovery ◽

10.1038/s41420-021-00599-6 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Ding Yan ◽

Xiaofen Li ◽

Qianqian Yang ◽

Qingtian Huang ◽

Leyi Yao ◽

...

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cancer Cells ◽

Cancer Cell ◽

Lung Cancer Cells ◽

Cancer Therapies ◽

Metal Compounds ◽

Cancer Cell Death ◽

Bax Protein ◽

Synthetic Derivative

AbstractDeubiquitinates (DUBs) have been suggested as novel promising targets for cancer therapies. Accumulating experimental evidence suggests that some metal compounds have the potential to induce cancer cell death via inhibition of DUBs. We previously reported that auranofin, a gold(I)-containing agent used for the treatment of rheumatoid arthritis in clinics, can induce cell death by inhibiting proteasomal DUBs in a series of cancer cell lines. Unfortunately, currently available gold compounds are not potent in inhibiting DUBs. Here, we report that: (i) aumdubin, a synthetic derivative of auranofin, exhibited stronger DUB-inhibiting and apoptosis-inducing activities than auranofin in lung cancer cells; (ii) aumdubin shows high affinity for mitochondrial DUB USP30; (iii) aumdubin induces apoptosis by increasing the ubiquitination and mitochondrial location of Bax protein; and (iv) USP30 inhibition may contribute to Bax-dependent apoptosis induced by aumdubin in lung cancer cells. These results suggest that gold(I)-containing agent aumdubin induces Bax-dependent apoptosis partly through inhibiting the mitochondrial DUB USP30, which could open new avenues for lung cancer therapy.

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Correction: Fluorinated thiazolidinols cause cell death in A549 lung cancer cells via PI3K/AKT/mTOR and MAPK/ERK signalling pathways

MedChemComm ◽

10.1039/c6md90027e ◽

2016 ◽

Vol 7 (6) ◽

pp. 1256-1256

Author(s):

Ravindra M. Kumbhare ◽

Tulshiram L. Dadmal ◽

Dinesh Kumar ◽

M. Janaki Ramaiah ◽

Anudeep Kota ◽

...

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cancer Cells ◽

Lung Cancer Cells ◽

Signalling Pathways ◽

A549 Lung

Correction for “Fluorinated thiazolidinols cause cell death in A549 lung cancer cells via PI3K/AKT/mTOR and MAPK/ERK signalling pathways” by Ravindra M. Kumbhare et al., Med. Chem. Commun., 2016, DOI: 10.1039/c5md00603a.

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