Shinu Ozaki
Prostate cancer is one of the most common malignant tumours in the world, and it can occur as a result of genetic mutations and their accumulation when the tumour progresses to an advanced stage. Because of the absence of distinct symptoms in the early stages of prostate cancer, most cancer patients are discovered at advanced stages where tumour cells respond poorly to chemotherapy. Furthermore, genetic alterations in prostate cancer increase tumour cell aggressiveness. Docetaxel and paclitaxel are well-known drugs for prostate tumour treatment, and they have a similar role in cancer therapy that is based on preventing depolymerization of microtubules, disrupting microtubule equilibrium, and causing a delay in cell cycle progression. The current review seeks to provide insight on the mechanisms behind paclitaxel and docetaxel resistance in prostate cancer. When oncogenic factors such as CD133 are upregulated and PTEN, a tumour suppressor, is downregulated, prostate tumour cells become more malignant and can develop medication resistance. Furthermore, phytochemicals have been used as anti-tumor agents to reduce chemoresistance in prostate cancer. Naringenin and lovastatin are two anti-tumor drugs that have been utilised to slow the development of prostate cancer and improve treatment sensitivity. Furthermore, nanostructures like polymeric micelles and nanobubbles have been used to deliver anti-tumor drugs while reducing the danger of chemoresistance development. The current review highlights these topics in order to bring fresh insight on reversing treatment resistance in prostate cancer.
KeywordsProstate cancer, Paclitaxel, Docetaxel, Chemoresistance, Targeted delivery, Nanoparticles
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