The Modulator of Apoptosis 1 (MOAP-1) protein, a crucial regulator of apoptosis, has recently attracted considerable interest in oncology research. Its potential as a therapeutic target in bladder, breast, and non-small cell lung cancer (NSCLC) offers intriguing new therapeutic approaches. This comprehensive review consolidated work on MOAP-1's role in cancer biology, notably as a therapeutic target. A systematic review was conducted by searching digital databases for studies. Based on inclusion and exclusion criteria, ten articles were thoroughly assessed. Emerging evidence links MOAP-1 to bladder cancer chemosensitivity and MOAP-1-dependent chemosensitization of breast cancer mediated by phenylquinazoline derivatives. In addition, apoptosis in breast cancer cells was induced by α-mangostin, a potential therapeutic drug targeting MOAP-1 and BCL-XL interaction. Studies showed MOAP-1's importance in NSCLC, with its upregulation in the cancer cells as a potential treatment. This review also highlights the role of miR-25 as a cellular regulator of MOAP-1 and its implication for MOAP-1-mediated therapeutics. The intricate control of MOAP-1 in cancer highlights the need for more research to understand its function and regulation across cancer types completely. MOAP-1's tumor suppressor activity suggests it could be a therapeutic target, as evidenced by current research findings, which is likely to spur further research into MOAP-1-targeted cancer treatments. This systematic review fills a gap in the literature by bringing together a variety of study findings to promote a deeper understanding of MOAP-1 and its therapeutic potential.

Cancer represents a significant global health concern, contributing to a high number of fatalities in the 21st century, with projections indicating a continuous spike in cancer cases. Although chemotherapy is an established cancer treatment, it is often associated with adverse effects and chemoresistance. Thus, alternative therapies like natural products that can address these limitations of chemotherapy are crucial. Alpha-mangostin (AM), derived from the mangosteen fruit, has widely demonstrated potent anticancer and enhanced chemosensitivity properties by regulating oncogenic signaling pathways, including phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), nuclear factor-κB (NF-κB), and mitogen-activated protein kinase (MAPK) pathways. This review discusses the current anticancer status of AM in preclinical studies and associated molecular mechanisms. It also further identifies the challenges and strategies to enhance the anticancer activity of AM. AM has shown strong anticancer effects in preclinical studies across multiple cancer types, including breast, cervical, ovarian, colorectal, pancreatic, prostate, and lung cancers. It induces apoptosis, causes cell cycle arrest, and inhibits the proliferation of cancer cells. AM also reduces cancer progression and metastasis by targeting key signaling pathways, demonstrating broad therapeutic potential. To overcome the limitations of AM, such as low bioavailability and limited clinical evidence, strategies like nanotechnology, chemical modification, and combination with chemotherapeutic agents have been proposed. These approaches aim to enhance AM's therapeutic potential. However, further research is needed to assess its pharmacokinetics, safety, and clinical efficacy. Future studies should also focus on improving delivery systems and conducting rigorous clinical trials to support AM’s use in integrative cancer therapy. Graphical Alpha-mangostin exerts anticancer effects by regulating cell cycle arrest, inhibiting tumorigenesis, metastasis, and cell proliferation, inducing apoptosis, and enhancing chemosensitivity. However, its therapeutic potential is limited by low solubility, bioavailability, and biodistribution, which could be improved through nanoparticle encapsulation, derivative synthesis, or combination with other chemotherapeutic agents.