Cellular signaling pathways involved in the maintenance of the equilibrium between cell proliferation and apoptosis have emerged as rational targets that can be exploited in the prevention and treatment of cancer. Epigallocatechin-3-gallate (EGCG) is the most abundant phenolic compound found in green tea. It has been shown to regulate multiple crucial cellular signaling pathways, including those mediated by EGFR, JAK-STAT, MAPKs, NF-κB, PI3K-AKT-mTOR, and others. Deregulation of the abovementioned pathways is involved in the pathophysiology of cancer. It has been demonstrated that EGCG may exert anti-proliferative, anti-inflammatory, and apoptosis-inducing effects or induce epigenetic changes. Furthermore, preclinical and clinical studies suggest that EGCG may be used in the treatment of numerous disorders, including cancer. This review aims to summarize the existing knowledge regarding the biological properties of EGCG, especially in the context of cancer treatment and prophylaxis.

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.

Ursolic acid (UA) is a pentacyclic triterpenoid frequently found in medicinal herbs and plants, having numerous pharmacological effects. UA and its analogs treat multiple diseases, including cancer, diabetic neuropathy, and inflammatory diseases. UA inhibits cancer proliferation, metastasis, angiogenesis, and induced cell death, scavenging free radicals and triggering numerous anti- and pro-apoptotic proteins. The biochemistry of UA has been examined broadly based on the literature, with alterations frequently having been prepared on positions C-3 (hydroxyl), C12–C13 (double bonds), and C-28 (carboxylic acid), leading to several UA derivatives with increased potency, bioavailability and water solubility. UA could be used as a protective agent to counter neural dysfunction via anti-oxidant and anti-inflammatory effects. It is a potential therapeutic drug implicated in the treatment of cancer and diabetic complications diseases provide novel machinery to the anti-inflammatory properties of UA. The pharmacological efficiency of UA is exhibited by the therapeutic theory of one-drug → several targets → one/multiple diseases. Hence, UA shows promising therapeutic potential for cancer and diabetic neuropathy diseases. This review aims to discuss mechanistic insights into promising beneficial effects of UA. We further explained the pharmacological aspects, clinical trials, and potential limitations of UA for the management of cancer and diabetic neuropathy diseases.

Background: Bax, a proapoptotic protein but its regulation during oral cancer progression and resistance remains elusive.Methods: A total of 127 samples including adjacent normal, primary tumor, and resistance to chemoradiation therapy (RCRT) samples from oral squamous cell carcinoma (OSCC) patients were used. The status of Bax was analyzed at DNA/mRNA/protein levels and the results were correlated with p53 and Akt expression in tissue samples/cisplatin‐resistant oral tongue SCC (SCC9/SCC4‐CisR) cell line.Results: Frequent progressive decrease of Bax expression with infrequent promoter methylation, polymorphisms G(‐248)A, and mutations was observed in OSCC progression/resistance. Furthermore, by targeting Akt pathway, induction of Bax‐dependent cell death was observed and this was further enhanced with nimbolide treatment in SCC9/SCC4‐CisR cells.Conclusion: Hence, the Bax gene alteration and its deregulation through p53/Akt pathway are important for OSCC progression and drug resistance. Akt Inhibitor VIII and nimbolide synergistically induce Bax, and it is therefore beneficial for chemosensitizing cisplatin‐resistant human OSCC.

Oxidative stress (OS), resulting from an imbalance between reactive oxygen species (ROS) and the antioxidant defense system, plays a critical role in the initiation and progression of cancer. Recent research has highlighted the regulatory influence of non-coding RNAs (ncRNAs) on cancer initiation and development through the regulation of redox homeostasis and key signaling pathways, which makes them potential targets for anticancer therapy. The ncRNA–oxidative stress axis contributes to malignancy through DNA damage, altered signaling, and dysregulated molecular networks. Plant-derived dietary components and phytochemicals have garnered significant attention for their ability to restore ROS balance and modulate the ncRNA/OS axis, thereby inhibiting carcinogenesis and enhancing the efficacy of chemotherapy. To study the interplay between OS, ncRNAs, and the anticancer potential of plant-derived compounds, in this review, we conducted an extensive search of electronic databases to identify and analyze studies that explore the interwork between OS, ncRNAs, and the chemotherapeutic role of phytochemicals. We discuss the dual role of phytochemicals in both cancer induction and suppression, emphasizing their capacity to generate ROS and regulate ncRNA expression. Furthermore, the review underscores the importance of nutritional interventions and antioxidant regulation in cancer chemoprevention and therapy, including the interconnected roles of oxidative stress, ncRNAs, and phytochemicals in cancer development and treatment, with a focus on dietary modulation as a strategic approach in oncology.