A state-of-art of underlying molecular mechanisms and pharmacological interventions/nanotherapeutics for cisplatin resistance in gastric cancer.

Autor: Gupta J; Institute of Pharmaceutical Research, GLA University, Mathura 281406, U.P., India., Ahmed AT; Department of Nursing, Al-Maarif University College, Ramadi, Anbar, Iraq. Electronic address: Abdulrahman.dheyab@uoa.edu.iq., Tayyib NA; Faculty of Nursing, Umm Al-Qura University, Makkah, Saudi Arabia., Zabibah RS; Medical Laboratory Technology Department, College of Medical Technology, The Islamic University, Najaf, Iraq., Shomurodov Q; Department of Maxillofacial Surgery, Tashkent State Dental Institute, Tashkent, Uzbekistan; Department of Scientific Affairs, Samarkand State Medical University, Samarkand, Uzbekistan., Kadheim MN; Department of Dentistry, Kut University College, Kut, Wasit 52001, Iraq; Medical Laboratory Techniques Department, Al-Farahidi University, Baghdad 10022 Iraq., Alsaikhan F; College of Pharmacy, Prince Sattam Bin Abdulaziz University, Alkharj, Saudi Arabia. Electronic address: fsaikhan@hotmail.com., Ramaiah P; Faculty of Nursing, Umm Al-Qura University, Makkah, Saudi Arabia., Chinnasamy L; College of Nursing, Riyadh Elm University, Riyadh, Saudi Arabia., Samarghandian S; Healthy Ageing Research Centre, Neyshabur University of Medical Sciences, Neyshabur, the Islamic Republic of Iran. Electronic address: samarghandians1@nums.ac.ir.
Jazyk: angličtina
Zdroj: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2023 Oct; Vol. 166, pp. 115337. Date of Electronic Publication: 2023 Sep 04.
DOI: 10.1016/j.biopha.2023.115337
Abstrakt: The fourth common reason of death among patients is gastric cancer (GC) and it is a dominant tumor type in Ease Asia. One of the problems in GC therapy is chemoresistance. Cisplatin (CP) is a platinum compound that causes DNA damage in reducing tumor progression and viability of cancer cells. However, due to hyperactivation of drug efflux pumps, dysregulation of genes and interactions in tumor microenvironment, tumor cells can develop resistance to CP chemotherapy. The current review focuses on the CP resistance emergence in GC cells with emphasizing on molecular pathways, pharmacological compounds for reversing chemoresistance and the role of nanostructures. Changes in cell death mechanisms such as upregulation of pro-survival autophagy can prevent CP-mediated apoptosis that results in drug resistance. Moreover, increase in metastasis via EMT induction induces CP resistance. Dysregulation of molecular pathways such as PTEN, PI3K/Akt, Nrf2 and others result in changes in CP response of GC cells. Non-coding RNAs determine CP response of GC cells and application of pharmacological compounds with activity distinct of CP can result in sensitivity in tumor cells. Due to efficacy of exosomes in transferring bioactive molecules such as RNA and DNA molecules among GC cells, exosomes can also result in CP resistance. One of the newest progresses in overcoming CP resistance in GC is application of nanoplatforms for delivery of CP in GC therapy that they can increase accumulation of CP at tumor site and by suppressing carcinogenic factors and overcoming biological barriers, they increase CP toxicity on cancer cells.
Competing Interests: Declaration of Competing Interest The authors declare that there are no conflicts of interest.
(Copyright © 2023. Published by Elsevier Masson SAS.)
Databáze: MEDLINE
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