Microbiology and Biotechnology Research: An Overview Vol. 8

Haematological malignancies, including leukaemia and lymphoma, represent a significant global health burden characterised by uncontrolled clonal expansion of lymphoid or myeloid cells. Telomerase, a ribonucleoprotein enzyme responsible for maintaining telomere integrity, is aberrantly upregulated in approximately 85–90% of all human cancers, including lymphoid and myeloid neoplasms, thereby conferring cellular immortality and resistance to apoptosis. Curcumin (diferuloylmethane), a polyphenolic compound derived from the rhizome of Curcuma longa, has attracted considerable scientific attention for its pleiotropic anticancer activities, including anti-proliferative, pro-apoptotic, anti-inflammatory, and anti-angiogenic properties. Despite a growing body of in vitro and in vivo experimental evidence supporting the anti-telomerase activity of curcumin in various cancer models, a comprehensive synthesis of this evidence in the specific context of lymphoma and leukaemia cells remains limited in the literature. This narrative review consolidates the current understanding of the mechanistic basis by which curcumin regulates telomerase activity in lymphoma and leukaemia cells, critically appraising the experimental evidence from both in vitro and in vivo studies and examining the synergistic potential of curcumin in combination with conventional antineoplastic agents. Emerging evidence suggests that curcumin can modulate telomerase activity through multiple converging molecular pathways, including the inhibition of nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (STAT3), phosphoinositide-3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR), and Wnt/β-catenin signalling, all of which are transcriptional regulators of the human telomerase reverse transcriptase (hTERT) gene. Additionally, curcumin may influence hTERT expression through epigenetic reprogramming, including DNA methylation and histone modification. Collectively, the evidence supports a model in which curcumin exerts multi-targeted suppression of telomerase activity through both transcriptional and post-translational mechanisms, further reinforced by epigenetic reprogramming. This review also identifies critical knowledge gaps and proposes future research directions to advance curcumin-based therapeutic strategies targeting telomerase in haematological malignancies.