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Sorcin a Potential Molecular Target for Cancer Therapy

Sorcin (Soluble resistance related calcium binding protein) is a small soluble penta EF family (PEF) of calcium (Ca(2+)) binding protein (22,000 Da). It has been reported to play crucial roles in the regulation of calcium homeostasis, apoptosis, vesicle trafficking, cancer development, and multidrug...

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Autores principales: Shabnam, Bano, Padmavathi, Ganesan, Banik, Kishore, Girisa, Sosmitha, Monisha, Javadi, Sethi, Gautam, Fan, Lu, Wang, Lingzhi, Mao, Xinliang, Kunnumakkara, Ajaikumar B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Neoplasia Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134165/
https://www.ncbi.nlm.nih.gov/pubmed/30216763
http://dx.doi.org/10.1016/j.tranon.2018.08.015
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author Shabnam, Bano
Padmavathi, Ganesan
Banik, Kishore
Girisa, Sosmitha
Monisha, Javadi
Sethi, Gautam
Fan, Lu
Wang, Lingzhi
Mao, Xinliang
Kunnumakkara, Ajaikumar B.
author_facet Shabnam, Bano
Padmavathi, Ganesan
Banik, Kishore
Girisa, Sosmitha
Monisha, Javadi
Sethi, Gautam
Fan, Lu
Wang, Lingzhi
Mao, Xinliang
Kunnumakkara, Ajaikumar B.
author_sort Shabnam, Bano
collection PubMed
description Sorcin (Soluble resistance related calcium binding protein) is a small soluble penta EF family (PEF) of calcium (Ca(2+)) binding protein (22,000 Da). It has been reported to play crucial roles in the regulation of calcium homeostasis, apoptosis, vesicle trafficking, cancer development, and multidrug resistance (MDR). Overexpression of sorcin has been reported to be associated with different cancers such as breast cancer, colorectal cancer, gastric cancer, leukemia, lung cancer, nasopharyngeal cancer, ovarian cancer, etc. Essentially, expression of sorcin has been found to be elevated in cancer cells as compared to normal cells, indicating that it has prominent role in cancer. Moreover, sorcin was found to be the regulator of various proteins that has an association with carcinogenesis including NF-κB, STAT3, Akt, ERK1/2, VEGF, MMPs, caspases, etc. Sorcin was also found to regulate apoptosis, as silencing of the same resulted in increased levels of proapoptotic genes and induced mitochondrial apoptotic pathway in cancer. Interestingly, mutations in the sorcin gene have been closely linked with poor overall survival in bladder cancer, brain lower-grade glioma, glioblastoma, glioblastoma multiforme, kidney renal clear cell carcinoma, and stomach adenocarcinoma. Additionally, overexpression of sorcin was also found to induce MDR against different chemotherapeutic drugs. All these findings mark the importance of sorcin in cancer development and MDR. Therefore, there is urgent need to explore the functional mechanism of sorcin and to analyze whether silencing of sorcin would able to chemosensitize MDR cells. The current review summarizes the structure, expression, and functions of sorcin and its importance in the regulation of various malignancies and MDR.
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spelling pubmed-61341652018-09-12 Sorcin a Potential Molecular Target for Cancer Therapy Shabnam, Bano Padmavathi, Ganesan Banik, Kishore Girisa, Sosmitha Monisha, Javadi Sethi, Gautam Fan, Lu Wang, Lingzhi Mao, Xinliang Kunnumakkara, Ajaikumar B. Transl Oncol Review article Sorcin (Soluble resistance related calcium binding protein) is a small soluble penta EF family (PEF) of calcium (Ca(2+)) binding protein (22,000 Da). It has been reported to play crucial roles in the regulation of calcium homeostasis, apoptosis, vesicle trafficking, cancer development, and multidrug resistance (MDR). Overexpression of sorcin has been reported to be associated with different cancers such as breast cancer, colorectal cancer, gastric cancer, leukemia, lung cancer, nasopharyngeal cancer, ovarian cancer, etc. Essentially, expression of sorcin has been found to be elevated in cancer cells as compared to normal cells, indicating that it has prominent role in cancer. Moreover, sorcin was found to be the regulator of various proteins that has an association with carcinogenesis including NF-κB, STAT3, Akt, ERK1/2, VEGF, MMPs, caspases, etc. Sorcin was also found to regulate apoptosis, as silencing of the same resulted in increased levels of proapoptotic genes and induced mitochondrial apoptotic pathway in cancer. Interestingly, mutations in the sorcin gene have been closely linked with poor overall survival in bladder cancer, brain lower-grade glioma, glioblastoma, glioblastoma multiforme, kidney renal clear cell carcinoma, and stomach adenocarcinoma. Additionally, overexpression of sorcin was also found to induce MDR against different chemotherapeutic drugs. All these findings mark the importance of sorcin in cancer development and MDR. Therefore, there is urgent need to explore the functional mechanism of sorcin and to analyze whether silencing of sorcin would able to chemosensitize MDR cells. The current review summarizes the structure, expression, and functions of sorcin and its importance in the regulation of various malignancies and MDR. Neoplasia Press 2018-09-11 /pmc/articles/PMC6134165/ /pubmed/30216763 http://dx.doi.org/10.1016/j.tranon.2018.08.015 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review article
Shabnam, Bano
Padmavathi, Ganesan
Banik, Kishore
Girisa, Sosmitha
Monisha, Javadi
Sethi, Gautam
Fan, Lu
Wang, Lingzhi
Mao, Xinliang
Kunnumakkara, Ajaikumar B.
Sorcin a Potential Molecular Target for Cancer Therapy
title Sorcin a Potential Molecular Target for Cancer Therapy
title_full Sorcin a Potential Molecular Target for Cancer Therapy
title_fullStr Sorcin a Potential Molecular Target for Cancer Therapy
title_full_unstemmed Sorcin a Potential Molecular Target for Cancer Therapy
title_short Sorcin a Potential Molecular Target for Cancer Therapy
title_sort sorcin a potential molecular target for cancer therapy
topic Review article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134165/
https://www.ncbi.nlm.nih.gov/pubmed/30216763
http://dx.doi.org/10.1016/j.tranon.2018.08.015
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