Cellular landscaping of cisplatin resistance in cervical cancer

Cervical cancer (CC) caused by human papillomavirus (HPV) is one of the largest causes of malignancies in women worldwide. Cisplatin is one of the widely used drugs for the treatment of CC is rendered ineffective owing to drug resistance. This review highlights the cause of resistance and the mechanism of cisplatin resistance cells in CC to develop therapeutic ventures and strategies that could be utilized to overcome the aforementioned issue. These strategies would include the application of nanocarries, miRNA, CRIPSR/Cas system, and chemotherapeutics in synergy with cisplatin to not only overcome the issues of drug resistance but also enhance its anti-cancer efficiency. Moreover, we have also discussed the signaling network of cisplatin resistance cells in CC that would provide insights to develop therapeutic target sites and inhibitors. Furthermore, we have discussed the role of CC metabolism on cisplatin resistance cells and the physical and biological factors affecting the tumor microenvironments.

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Bibliographic Details
Main Authors: Bhattacharjeea, Rahul, Deya, Tanima, Kumar, Lamha, Kar, Sulagna, Sarkar, Ritayan, Ghorai, Mimosa, Malik, Sumira, Jha, Niraj K., Vellingiri, Balachandar, Kumar Kesari, Kavindra, Pérez de Lastra, José Manuel, Dey, Abhijit
Other Authors: Agencia Canaria de Investigación, Innovación y Sociedad de la Información
Format: artículo biblioteca
Language:English
Published: Elsevier 2022-07-08
Subjects:Cervical cancer, cisplatin resistance, drug resistance, anti-cancer activity, chemotherapeutics, tumor microenvironment, cell signaling,
Online Access:http://hdl.handle.net/10261/279183
http://dx.doi.org/10.13039/501100007757
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Summary:Cervical cancer (CC) caused by human papillomavirus (HPV) is one of the largest causes of malignancies in women worldwide. Cisplatin is one of the widely used drugs for the treatment of CC is rendered ineffective owing to drug resistance. This review highlights the cause of resistance and the mechanism of cisplatin resistance cells in CC to develop therapeutic ventures and strategies that could be utilized to overcome the aforementioned issue. These strategies would include the application of nanocarries, miRNA, CRIPSR/Cas system, and chemotherapeutics in synergy with cisplatin to not only overcome the issues of drug resistance but also enhance its anti-cancer efficiency. Moreover, we have also discussed the signaling network of cisplatin resistance cells in CC that would provide insights to develop therapeutic target sites and inhibitors. Furthermore, we have discussed the role of CC metabolism on cisplatin resistance cells and the physical and biological factors affecting the tumor microenvironments.