Therapeutic potential of autophagy activators and inhibitors in lung and breast cancer- a review.

Mol Biol Rep

School of Biotechnology and Bioinformatics, DY Patil Deemed to Be University, CBD Belapur, 400614, Navi Mumbai, Maharashtra, India.

Published: November 2022

Autophagy is a cellular process that eliminates damaged components of cytoplasm via the lysosome. Autophagy supports cells and tissues to remain healthy by recycling old or damaged cellular organelles and proteins with new ones. The breakdown products that follow are directed into cellular metabolism, where they are utilized to produce energy as well as for maintaining homeostasis and stability of the genome. In many cancers, autophagy modulation carries out a dual role in cancer development and suppression. Autophagy suppresses the proliferation of cancer cells by bringing about cell death and limiting cancer cell development, although it also promotes tumorigenesis by encouraging cancer cell growth and formation. Nevertheless, autophagy's implication in cancer remains a paradox. While several autophagy activators, and inhibitors, such as SAH-EJ2, Gefitinib, Ampelopsin hydroxychloroquine and chloroquine, are utilized to regulate autophagy in chemoprevention, the exact intrinsic system of autophagy in cancer deserves further investigation. Despite improved treatment regimens, the incidence rate of both breast and lung cancer has grown, as has the number of recurrence cases. Hence, this review offers a wide overview of autophagy's underlying role in lung and breast cancer, particularly focusing on the various autophagy activators and inhibitors in both cancers, as well as the use of various organic compounds, regular drugs, and natural products in cancer prevention and treatment.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11033-022-07711-8DOI Listing

Publication Analysis

Top Keywords

autophagy activators
12
activators inhibitors
12
autophagy
9
cancer
9
lung breast
8
cancer cell
8
therapeutic potential
4
potential autophagy
4
inhibitors lung
4
breast cancer-
4

Similar Publications

Pancreatic cancer is an aggressive tumor, which is often associated with a poor clinical prognosis and resistance to conventional chemotherapy. Therefore, there is a need to identify new therapeutic markers for pancreatic cancer. Although KIN17 is a highly expressed DNA‑ and RNA‑binding protein in a number of types of human cancer, its role in pancreatic cancer development, especially in relation to progression, is currently unknown.

View Article and Find Full Text PDF

Gengnianchun Against HO-Induced Oxidative Damage in KGN Cells via miR-548m/FOXO3 Signaling.

J Cell Biochem

January 2025

Department of Integrated Traditional Chinese Medicine and Western Medicine, The Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.

Gengnianchun (GNC) is a traditional remedy used for diminished ovarian reserve, but its underlying mechanisms remain unclear. This study aimed to explore these mechanisms in human granulosa-like cancer (KGN) cells pretreated with medicated rat serum (MRS) before HO exposure. MRS pretreatment significantly alleviated HO-induced cell damage, including improvements in cell viability, superoxide dismutase and GSH-Px activities, and Bcl-2 expression.

View Article and Find Full Text PDF

Protective mechanism of safflower yellow injection on myocardial ischemia-reperfusion injury in rats by activating NLRP3 inflammasome.

BMC Complement Med Ther

January 2025

Institute of Basic Medical Sciences of Xiyuan Hospital, Beijing Key Laboratory of Chinese Materia Pharmacology, China Academy of Chinese Medical Sciences, National Clinical Research Center of Traditional Chinese Medicine for Cardiovascular Diseases, Beijing, China.

Objectives: This study intended to explore whether the protective effect safflower yellow injection (SYI) on myocardial ischemia-reperfusion (I/R) injury in rats mediated of the NLRP3 inflammasome signaling.

Methods: The I/R model was prepared by ligating the left anterior descending coronary artery for 45 min and then releasing the blood flow for 150 min. 96 male Wistar rats were randomly divided into sham group, I/R group, Hebeishuang group (HBS), SYI high-dose group (I/R + SYI-H), SYI medium-dose group (I/R + SYI-M) and SYI low-dose group (I/R + SYI-L).

View Article and Find Full Text PDF

High glucose induces renal tubular epithelial cell senescence by inhibiting autophagic flux.

Hum Cell

January 2025

Department of Nephrology, Zhong Da Hospital, Gulou District, No. 87, Dingjiaqiao, Zhongyangmen Street, Nanjing, 210009, Jiangsu, China.

Autophagy, a cellular degradation process involving the formation and clearance of autophagosomes, is mediated by autophagic proteins, such as microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (p62), and modulated by 3-methyladenine (3-MA) as well as chloroquine (CQ). Senescence, characterised by permanent cell cycle arrest, is marked by proteins such as cyclin-dependent kinase inhibitor 1 (p21) and tumour protein 53 (p53). This study aims to investigate the relationship between cell senescence and renal function in diabetic kidney disease (DKD) and the effect of autophagy on high-glucose-induced cell senescence.

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!