Anti-Proliferative and Pro-Apoptotic Effects ofCalligonum comosum(L’Her.) Methanolic Extract in Human Triple-Negative MDA-MB-231 Breast Cancer Cells

Abstract

Triple-negative breast cancer (TNBC), the most aggressive subtype, does not respond to targeted therapy due to the lack of hormone receptors. There is an urgent need for alternative therapies, including natural product-based anti-cancer drugs, at lower cost. We investigated the impact of a Calligonum comosum L’Hér. methanolic extract (CcME) on the TNBC MDA-MB-231 cell line proliferation and related cell death mechanisms performing cell viability and cytotoxicity assays, flow cytometry to detect apoptosis and cell cycle analysis. The apoptosis-related protein array and cellular reactive oxygen species (ROS) assay were also carried out. We showed that the CcME inhibited the TNBC cell viability, in a dose-dependent manner, with low cytotoxic effects. The CcME-treated TNBC cells underwent apoptosis, associated with a concomitant increase of apoptosis-related protein expression, including cytochrome c, cleaved caspase-3, cyclin-dependent kinase inhibitor p21, and the anti-oxidant enzyme catalase, compared with the untreated cells. The CcME also enhanced the mitochondrial transition pore opening activity and induced G0/G1 cell growth arrest, which confirmed the cytochrome c release and the increase of the p21 expression detected in the CcME-treated TNBC cells. The CcME-treated TNBC cells resulted in intracellular ROS production, which, when blocked with a ROS scavenger, did not reduce the CcME-induced apoptosis. In conclusion, CcME exerts anti-proliferative effects against TNBC cells through the induction of apoptosis and cell growth arrest. In vivo studies are justified to verify the CcME anti-proliferative activities and to investigate any potential anti-metastatic activities of CcME against TNBC development and progression.

The Natural Products and Extracts: Anti‐Triple‐Negative Breast Cancer in Vitro

“…Compared with the untreated cells, the CcME‐treated TNBC cells underwent apoptosis, associated with a concomitant increase of apoptosis‐related protein expression, like cytochrome c, cleaved caspase‐3, cyclin‐dependent kinase inhibitor p21, and the anti‐oxidant enzyme catalase. It also enhanced the mitochondrial transition pore opening activity, induced G0/G1 cell growth arrest and increased intracellular ROS production [86] …”

“…It also enhanced the mitochondrial transition pore opening activity, induced G0/G1 cell growth arrest and increased intracellular ROS production. [86] Annona muricata L. (A. muricata or AM) possessed a lot of active constituents like acetogenins, alkaloids, phenols and so on. The Annona muricata ethyl acetate (AMEA) decreased the BT-20 TNBC cell viability in a concentration and time-dependent manner compared to the control.…”

Commiphora myrrha (Nees) Engl. resin extracts induce phase-I cytochrome P450 2C8, 2C9, 2C19, and 3A4 isoenzyme expressions in human hepatocellular carcinoma (HepG2) cells

“…The method was applied as previously described in Alehaideb et al (2020) with modifications. Briefly, protein samples (120 µg per well) were separated on 11 percent SDS–polyacrylamide gels and electro-blotted onto a Thermo Fisher polyvinylidene difluoride (PVDF) transfer membrane 0.45 μm (catalog number, #88518).…”

Bursatella leachii purple ink secretion extract exerts cytotoxic properties against human hepatocarcinoma cell line (HepG2): In vitro and in silico studies

“…After 24 h of incubation, the cells were treated in triplicates with B. leachii extract at 100 and 400 µg/mL along with 1 µM STS, used as a positive control. Western blot technology and image analysis were employed as previously described in [35]. Polyvinylidene di uoride membranes (Millipore, Thermo Fisher Scienti c)…”