The critical role of NLRP3 in drug resistance of cancers: Focus on the molecular mechanisms and possible therapeutics

被引：1

作者：

Kuriakose, Beena Briget ^{[1
]}

Zwamel, Ahmed Hussein ^{[2
,3
,4
]}

Mutar, Ayad Abdulrazzaq ^{[5
]}

Uthirapathy, Subasini ^{[6
]}

Bishoyi, Ashok Kumar ^{[7
]}

Naidu, K. Satyam ^{[8
]}

Hjazi, Ahmed ^{[9
]}

Nakash, Prashant ^{[10
]}

Arya, Renu ^{[11
]}

Almalki, Sami G. ^{[12
]}

机构：

[1] King Khalid Univ, Coll Appl Med Sci, Dept Basic Med Sci, Khamis Mushayt, Saudi Arabia

[2] Islamic Univ, Coll Med & Tech, Dept Med Lab Tech, Najaf, Iraq

[3] Islamic Univ Al Diwaniyah, Med Lab Tech Coll, Dept Med Anal, Al Diwaniyah, Iraq

[4] Islamic Univ Babylon, Med Lab Tech Coll, Dept Med Anal, Babylon, Iraq

[5] Al Maarif Univ, Coll Hlth & Med Technol, Dept Med Labs Tech, Anbar, Iraq

[6] Tishk Int Univ, Pharm Dept, Erbil, Kurdistan Regio, Iraq

[7] Marwadi Univ, Res Ctr, Fac Sci, Dept Microbiol, Rajkot, Gujarat, India

[8] Raghu Engn Coll, Dept Chem, Visakhapatnam, Andhra Prades, India

[9] Prince Sattam Bin Abdulaziz Univ, Coll Appl Med Sci, Dept Med Lab, Al Kharj, Saudi Arabia

[10] NIMS Univ Rajasthan, NIMS Inst Pharm, Jaipur, Rajasthan, India

[11] Chandigarh Grp Coll Jhanjeri, Chandigarh Pharm Coll, Mohali, Punjab, India

[12] Majmaah Univ, Coll Appl Med Sci, Dept Med Lab Sci, Majmaah, Saudi Arabia

来源：

SEMINARS IN ONCOLOGY | 2025年 / 52卷 / 01期

关键词：

NLRP3; Cancer; Drug resistance; Inflammation; Treatment; INFLAMMASOME ACTIVATION; KAPPA-B; CELLS; CISPLATIN; COLITIS; PATHWAY; INHIBITOR; APOPTOSIS; RECEPTOR; ACID;

D O I：

10.1016/j.seminoncol.2025.152337

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Nod-like receptor protein 3 (NLRP3) is a member of the leucine-rich repeat-containing protein (NLR) canonical inflammasome family. It regulates the pathophysiology of cancer by facilitating immune responses and apoptotic proteins. Furthermore, it has been observed that chemotherapy activates NLRP3 in human malignancies. The secretion of IL-1 8 and IL-22 to promote cancer spread may be triggered by NLRP3 activation. Furthermore, earlier studies have exhibited that NLRP3 may cause medication resistance when used in cancer treatments given that cell viability may be regulated by NLRP3 depletion. Additionally, clinical studies have demonstrated correlation between NLRP3 expression, lymphogenesis, and cancer metastasis. Various NLRP3 agonists may cause the EMT process, stimulate IL-1 8 and Wnt/ 8catenin signaling, and alter miRNA function in drug-resistant cells. This review seeks to clarify the possibility involvement of NLRP3-related pathways in the control of cancer cells' resistance to widely used treatment approaches, such as chemotherapy. In the end, an improved perception of the corresponding mechanisms behind NLRP3' s tumor-supporting activities will help NLRP3-based treatments advance in the future. (c) 2025 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

引用

页码：27 / 40

页数：14

共 178 条

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