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Antiglycolytic Activities of Strobilanthes crispus Active Fraction and its Bioactive Components on Triple-Negative Breast Cancer Cells In Vitro

Muhammad SNH, Yaacob NS, Safuwan NAM, Fauzi AN

Anticancer Agents Med Chem, 2021 Apr 26.
PMID: 33906591 DOI: 10.2174/1871520621666210427104804

BACKGROUND: Survival and progression of cancer cells are highly dependent on aerobic glycolysis. Strobilanthes crispus has been shown to have promising anticancer effects on breast cancer cells. The involvement of the glycolysis pathway in producing these effects is unconfirmed, thus further investigation is required to elucidate this phenomenon.
OBJECTIVE: This study aims to determine the effect of S. crispus active fraction (F3) and its bioactive components on glycolysis in triple-negative breast cancer cells (MDA-MB-231).
METHODS: This study utilizes F3, lutein, β-sitosterol, and stigmasterol to be administered in MDA-MB-231 cells for measurement of antiglycolytic activities through cell poliferation, glucose uptake, and lactate concentration assays. Cell proliferation was assessed by MTT assay of MDA-MB-231 cells after treatment with F3 and its bioactive components lutein, β-sitosterol, and stigmasterol. The IC50 value in each compound was determined by MTT assay to be used in subsequent assays. The determination of glucose uptake activity and lactate concentration were quantified using fluorescence spectrophotometry.
RESULTS: Antiproliferative activities were observed for F3 and its bioactive components, with IC50 values of 100 µg/mL (F3), 20 µM (lutein), 25 µM (β-sitosterol), and 90 μM (stigmasterol) in MDA-MB-231 cells at 48 h. The percentage of glucose uptake and lactate concentration in MDA-MB-231 cells treated with F3, lutein, or β sitosterol were significantly lower than those observed in the untreated cells in a time-dependent manner. However, treatment with stigmasterol decreased the concentration of lactate without affecting the glucose uptake in MDA-MB-231 cells.
CONCLUSION: The antiglycolytic activities of F3 on MDA-MB-231 cells are attributed to its bioactive components.
Terpenoids: Unlocking Their Potential on Cancer Glucose Metabolism

Muhammad SNH, Ramli RR, Nik Mohamed Kamal NNS, Fauzi AN

Phytother Res, 2024 Dec;38(12):5626-5640.
PMID: 39300823 DOI: 10.1002/ptr.8346

Cancer incidence has increased globally and has become the leading cause of death in the majority of countries. Many cancers have altered energy metabolism pathways, such as increased glucose uptake and glycolysis, as well as decreased oxidative phosphorylation. This is known as the Warburg effect, where cancer cells become more reliant on glucose to generate energy and produce lactate as an end product, even when oxygen is present. These are attributed to the overexpression of key glycolytic enzymes, glucose transporters, and related signaling pathways that occur in cancer cells. Therefore, overcoming metabolic alterations in cancer cells has recently become a target for therapeutic approaches. Natural products have played a key role in drug discovery, especially for cancer and infectious diseases. In this review, we are going to focus on terpenoids, which are gradually gaining popularity among drug researchers due to their reported anti-cancer effects via cell cycle arrest, induction of apoptosis, reduction of proliferation, and metastasis. This review summarizes the potential of 13 terpenoid compounds as anti-glycolytic inhibitors in different cancer models, primarily by inhibiting the glucose uptake and the generation of lactate, as well as by downregulating enzymes associated to glycolysis. As a conclusion, disruption of cancer cell glycolysis may be responsible for the anti-cancer activity of terpenoids.
Lutein reverses M2 macrophages polarization and exhibits antitumor effects on human triple-negative breast cancer cells

Ramli RR, Muhammad SNH, Azlan M, Nurul AA, Nafi SNM, Fauzi AN

Mol Biol Rep, 2026 Jan 16;53(1):295.
PMID: 41543578 DOI: 10.1007/s11033-026-11445-2

BACKGROUND: Triple-negative breast cancer (TNBC) remains a major therapeutic challenge due to the lack of established molecular targets and the presence of highly infiltrating tumor-associated macrophages (TAMs), particularly the immunosuppressive M2 phenotype that drives tumor progression. This study investigated the potential of lutein, a plant-derived carotenoid with anticancer properties, to repolarize human monocyte-derived M2 macrophages into the antitumor M1 phenotype and thereby modulate the TNBC tumor microenvironment.
METHODS AND RESULTS: CD14 + monocytes isolated from peripheral blood mononuclear cells were differentiated into M1 or M2 macrophages using GM-CSF/IFN-γ/lipopolysaccharide or M-CSF/IL-4, respectively. Lutein's effects on macrophage polarization, cell proliferation, cell migration and cytokine secretion were evaluated using flow cytometry, MTT proliferation assays, migration assays and enzyme-linked immunosorbent assays (ELISAs) in MDA-MB-231 cells. Additionally, tumor-related protein expressions from MDA-MB-231 cells were analyzed using protein arrays. Lutein significantly reduced the proliferation and migration of MDA-MB-231 cells when co-cultured with M1/M2 macrophages compared to the untreated group. IL-4 stimulation increased the expression of M2 macrophage marker (CD206) and protumor cytokines (IL-10 and TGF-β1), but lutein effectively reduced these elevated molecules in IL-4-activated macrophages. Proteomic profiling revealed that lutein downregulated several protumor proteins (survivin, VEGF, BCL-X, M-CSF, MMP-9) and upregulated antitumor markers (FKHR and GM-CSF). Furthermore, lutein markedly reduced the secretion of proinflammatory and protumorigenic cytokines and chemokines (IL-6, IL-18BPa, CCL2, CCL8, CCL7, CCL3, CCL20, and CXCL8).
CONCLUSION: These findings suggest that lutein reprograms M2 macrophages toward an M1-like phenotype and disrupts tumor-promoting signaling within the TNBC microenvironment, highlighting its potential as an adjunct therapeutic agent.

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