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B Cell Lymphoma 2: A Potential Therapeutic Target for Cancer Therapy
- Alam, M.;
- Ali, S.;
- Mohammad, T.;
- Hasan, G.M.;
- Yadav, D.K.;
- 외 1명
WEB OF SCIENCE
74SCOPUS
87초록
Defects in the apoptosis mechanism stimulate cancer cell growth and survival. B cell lymphoma 2 (Bcl-2) is an anti-apoptotic molecule that plays a central role in apoptosis. Bcl-2 is the founding constituent of the Bcl-2 protein family of apoptosis controllers, the primary apoptosis regulators linked with cancer. Bcl-2 has been identified as being over-expressed in several cancers. Bcl-2 is induced by protein kinases and several signaling molecules which stimulate cancer development. Identifying the important function played by Bcl-2 in cancer progression and development, and treatment made it a target related to therapy for multiple cancers. Among the various strategies that have been proposed to block Bcl-2, BH3-mimetics have appeared as a novel group of compounds thanks to their favorable effects on many cancers within several clinical settings. Because of the fundamental function of Bcl-2 in the regulation of apoptosis, the Bcl-2 protein is a potent target for the development of novel anti-tumor treatments. Bcl-2 inhibitors have been used against several cancers and provide a pre-clinical platform for testing novel therapeutic drugs. Clinical trials of multiple investigational agents targeting Bcl-2 are ongoing. This review discusses the role of Bcl-2 in cancer development; it could be exploited as a potential target for developing novel therapeutic strategies to combat various types of cancers. We further highlight the therapeutic activity of Bcl-2 inhibitors and their implications for the therapeutic management of cancer. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
키워드
- 제목
- B Cell Lymphoma 2: A Potential Therapeutic Target for Cancer Therapy
- 저자
- Alam, M.; Ali, S.; Mohammad, T.; Hasan, G.M.; Yadav, D.K.; Hassan, M.I.
- 발행일
- 2021-10
- 유형
- Review
- 권
- 22
- 호
- 19
- 언어
- ENG
- 출판사
- MDPI
- 발행국가
- 스위스
- ISSN
- E 1422-0067
P 1661-6596