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3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells

Verma M, Fatima S, Syed A, Elgorban AM, Abid I, Wong LS, et al.

Naunyn Schmiedebergs Arch Pharmacol, 2025 Feb 22.
PMID: 39985578 DOI: 10.1007/s00210-025-03899-1

Studies on the assessment of anticancer efficacy of plant-derived phytochemicals by targeting signaling pathways have drawn a lot of attention recently for human health. Multiple investigations have proposed an involvement of Notch pathway in the processes of cancer angiogenesis and metastasis, and drug resistance. Moreover, overexpression of Notch signaling is associated with increased prostate cancer (PrCa) cell growth and development. A number of chemotherapeutic agents are reported to become resistant over a period of time and have severe side effects. To increase efficacy and lessen drug-induced toxicity, a variety of bioactive compounds have been utilized alone or as adjuncts to traditional chemotherapy. Therefore, in the present study, the potential of AKBA in inhibiting the proliferation of PrCa cells by modulating Notch signaling components and its efficacy in combination with cisplatin was investigated. The results exhibited a substantial reduction in cell survival (IC50 = 25.28 µM at 24 h and 16.50 µM at 48 h) and cellular alterations in AKBA-treated PrCa cells. Additionally, AKBA caused nuclear condensation, increased reactive oxygen species (ROS) generation, mitochondrial membrane depolarization, and caspase activation, ultimately leading to apoptosis in PrCa cells. Moreover, AKBA-elicited apoptosis was evidenced by an augmentation in the Bax to Bcl2 ratio. AKBA was also found to induce G0/G1 arrest which was substantiated by reduced cyclin D1 and CDK4 expression levels concomitantly with increased expression of p21 and p27 genes. Intriguingly, AKBA demonstrated significant downregulation of Notch signaling mediators. Furthermore, the isobolograms of the combination treatment indicated that AKBA has the potential to synergistically enhance the cytotoxic efficacy of cisplatin in DU145 cells, as evidenced by CI
Expressions of selected microRNAs in gastric cancer patients and their association with Helicobacter pylori and its cag pathogenicity island

Rai RP, Syed A, Elgorban AM, Abid I, Wong LS, Khan MS, et al.

Microb Pathog, 2025 May;202:107442.
PMID: 40049249 DOI: 10.1016/j.micpath.2025.107442

BACKGROUND: Helicobacter pylori infection and the resulting inflammation of the stomach are widely recognized as the primary risk factors for the development of gastric cancer (human health). Despite numerous attempts, the correlation between various virulence factors of H. pylori and stomach cancer remains mainly unexplained. The cag pathogenicity island (cagPAI) is a widely recognized indicator of virulence in H. pylori. MicroRNAs play crucial roles in a wide range of biological and pathological processes and dysregulated expressions of miRNAs have been detected in numerous cancer types. However, research on the correlation between H. pylori infection and its cagPAI, as well as the differential expression of microRNAs in gastric cancer, is lacking.
AIM: The aim of this study was to examine the differential expression of miRNAs in 80 patients with gastric cancer, specifically in connection to the presence of H. pylori and its cag pathogenicity island (cagPAI).
METHODS: Biopsies of 80 gastric cancer patients were collected and used for H. pylori DNA isolation and tissue miRNA isolation, and further analyzed for cagPAI and miRNA expression and their association.
RESULTS: Elevated levels of miR-21, miR-155, and miR-223 were detected in malignant tissues. The expression of miR-21 and miR-223 was considerably elevated in biopsies that tested positive for H. pylori, whereas the expression of miR-34a was reduced. H. pylori cagPAI samples that are functionally intact exhibit greater expression of miR-21 and miR-223 compared to cagPAI samples that are partially deleted, in both normal and malignant tissues.
CONCLUSION: Thus, the novelty of our study lies in its focus on the differential expression of specific miRNAs in relation to the functional integrity of the cagPAI in H. pylori-infected gastric cancer patients, offering a more detailed understanding of the interplay between H. pylori virulence factors and miRNA regulation than previous studies.

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