Juice Alleviated Breast Cancer by Triggering the Mitochondrial Apoptosis Pathway and Suppressing the Jak2/Stat3 Pathway.

Nutrients

West China School of Public Health and West China Fourth Hospital, Sichuan University, 17# 3rd Section, Ren Min South Road, Chengdu 610041, China.

Published: August 2024

(RS) is a characteristic fruit in southwestern China that has numerous health benefits; however, its pharmacological effect needs further clarification, especially with respect to the exploration of its potential anti-breast-cancer effect, as there are still knowledge gaps in this regard. This study was designed to investigate the protective effects of juice (RSJ) on breast cancer (BC) through in vitro cellular experiments and by establishing mouse 4T1 breast xenograft tumors. This study also had the aim of elucidating RSJ's underlying mechanisms. RSJ can inhibit cell proliferation, affect cell morphology, and impact the clone formation ability of BC; furthermore, it can promote apoptosis by triggering the mitochondrial apoptosis pathway. In mouse 4T1 breast xenograft tumors, RSJ markedly inhibited tumor growth, relieved the pathological lesions, lowered the expression of Ki67, and regulated the expression of the apoptosis-associated protein. Moreover, we observed that RSJ can inhibit the Jak2/Stat3 signaling pathway both in vivo and in vitro. Overall, our research reveals that RSJ can alleviate BC by triggering the mitochondrial apoptosis pathway and suppressing the Jak2/Stat3 pathway, providing new dietary intervention strategies for BC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11357216PMC
http://dx.doi.org/10.3390/nu16162784DOI Listing

Publication Analysis

Top Keywords

triggering mitochondrial
12
mitochondrial apoptosis
12
apoptosis pathway
12
breast cancer
8
pathway suppressing
8
suppressing jak2/stat3
8
jak2/stat3 pathway
8
mouse 4t1
8
4t1 breast
8
breast xenograft
8

Similar Publications

Neural differentiation in perspective: mitochondria as early programmers.

Front Neurosci

January 2025

IDR/Research and Education Network, Westmead, NSW, Australia.

Neural differentiation during development of the nervous system has been extensively studied for decades. These efforts have culminated in the generation of a detailed map of developmental events that appear to be associated with emergence of committed cells in the nervous system. In this review the landscape of neural differentiation is revisited by focusing on abiotic signals that play a role in induction of neural differentiation.

View Article and Find Full Text PDF

Lidocaine could promote the cuproptosis through up-regulating the long noncoding RNA DNMBP-AS1 in Hep-2 cells.

BMC Cancer

January 2025

Department of Anesthesiology, the First Affiliated Hospital of Dalian Medical University, 222, Zhongshan Road, Xigang District, Dalian, 116011, Liaoning, China.

Background: Lidocaine is a traditional local anesthetic, which has been reported to trigger apoptosis through the mitochondrial pathway, independent of death receptor signaling. Cuproptosis is a copper triggered mitochondrial cell death mode. In this study, we explored the biological effects of lidocaine on cuproptosis in Hep-2 cells and studied the relevant mechanisms.

View Article and Find Full Text PDF

Mitochondrial NAD deficiency in vascular smooth muscle impairs collagen III turnover to trigger thoracic and abdominal aortic aneurysm.

Nat Cardiovasc Res

January 2025

Shanghai Fifth People's Hospital and Institutes of Biomedical Sciences Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.

Thoracic and abdominal aortic aneurysm poses a substantial mortality risk in adults, yet many of its underlying factors remain unidentified. Here, we identify mitochondrial nicotinamide adenine dinucleotide (NAD)⁺ deficiency as a causal factor for the development of aortic aneurysm. Multiomics analysis of 150 surgical aortic specimens indicated impaired NAD salvage and mitochondrial transport in human thoracic aortic aneurysm, with expression of the NAD transporter SLC25A51 inversely correlating with disease severity and postoperative progression.

View Article and Find Full Text PDF

Ecotoxicological impact of succinate dehydrogenase inhibitor (SDHI) fungicides on non-targeted organisms: a review.

Ecotoxicology

January 2025

Amity Institute of Environmental Sciences, Amity University, Sector-125, Noida, 201301, Uttar Pradesh, India.

As the global population continues to grow, the use of pesticides to increase food production is projected to escalate. Pesticides are critical in plant protection, offering a powerful defense against fungal diseases such as apple scab, leaf spot, sclerotinia rot, damping off, sheath blight, and root rot, which threaten crops like cereals, corn, cotton, soybean, sugarcane, tuberous vegetables, and ornamentals. Succinate Dehydrogenase Inhibitor (SDHI) fungicides represent a novel class essential for controlling fungal pathogens and bolstering food security.

View Article and Find Full Text PDF

The role of GPR81-cAMP-PKA pathway in endurance training-induced intramuscular triglyceride accumulation and mitochondrial content changes in rats.

J Physiol Sci

January 2025

Institute of Sports Science, Sichuan University, Chengdu, People's Republic of China; School of Physical Education and Sports, Sichuan University, Chengdu, People's Republic of China; Department of Physical Education, Sichuan University, No. 24 South Section 1, Yihuan Road, 610065, Chengdu, China. Electronic address:

The athlete's paradox phenomenon involves the accumulation of intramuscular triglycerides (IMTG) in both insulin-resistant and insulin-sensitive endurance athletes. Nevertheless, a complete understanding of this phenomenon is yet to be achieved. Recent research indicates that lactate, a common byproduct of physical activity, may increase the accumulation of IMTG in skeletal muscle.

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!