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Review
, 11 (12)

Mechanistic Understanding of Curcumin's Therapeutic Effects in Lung Cancer

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Review

Mechanistic Understanding of Curcumin's Therapeutic Effects in Lung Cancer

Wan Nur Baitty Wan Mohd Tajuddin et al. Nutrients.

Abstract

Lung cancer is among the most common cancers with a high mortality rate worldwide. Despite the significant advances in diagnostic and therapeutic approaches, lung cancer prognoses and survival rates remain poor due to late diagnosis, drug resistance, and adverse effects. Therefore, new intervention therapies, such as the use of natural compounds with decreased toxicities, have been considered in lung cancer therapy. Curcumin, a natural occurring polyphenol derived from turmeric (Curcuma longa) has been studied extensively in recent years for its therapeutic effects. It has been shown that curcumin demonstrates anti-cancer effects in lung cancer through various mechanisms, including inhibition of cell proliferation, invasion, and metastasis, induction of apoptosis, epigenetic alterations, and regulation of microRNA expression. Several in vitro and in vivo studies have shown that these mechanisms are modulated by multiple molecular targets such as STAT3, EGFR, FOXO3a, TGF-β, eIF2α, COX-2, Bcl-2, PI3KAkt/mTOR, ROS, Fas/FasL, Cdc42, E-cadherin, MMPs, and adiponectin. In addition, limitations, strategies to overcome curcumin bioavailability, and potential side effects as well as clinical trials were also reviewed.

Keywords: anti-cancer; curcumin; lung cancer; molecular mechanism.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Molecular targets of curcumin in inhibiting cell proliferation of lung cancer cells. The green arrow indicates upregulation, while the red arrow indicates downregulation of molecular targets. STAT 3: Signal transducer and activator of Transcription 3; eIF2α: Eukaryotic initiation factors 2 alpha; EGFR: Epidermal growth factor receptor; Foxo3a: Forkhead box class O; FOXA2; Forkhead box transcription factor A2; UBE1l: Ubiquitin-like modifier-activating enzyme; C-myc: C-myc proto-oncogene.
Figure 2
Figure 2
Molecular targets of curcumin in inducing cell apoptosis of lung cancer cells. The green arrow indicates upregulation, while the red arrow indicates downregulation of molecular targets. NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; COX-2: cyclooxygenase-2; ERK1/2: extra-cellular signal regulated kinase: ROS: reactive oxygen species; MAPK: mitogen-activated protein kinase; JNK: Jun N-terminal kinase; PI3K: phosphatidylinositol 3-kinase; Akt: protein kinase; mTOR: mammalian target of rapamycin; Bad: Bcl-2-associated death promoter; Bcl-2: B-cell lymphoma-2; BCL-xL: B-cell lymphoma-extra large; MCL1: induced myeloid leukemia cell differentiation protein; FADD: Fas-associated protein with death domain.
Figure 3
Figure 3
Molecular mechanism of anti-metastasis effect by curcumin against lung cancer cells. The green arrow indicates upregulation, while the red arrow indicates downregulation of molecular targets. VEGF: vascular endothelial growth factor; MMP-2: matrix metalloproteinase; MMP-9: matrix metalloproteinase-9; Cdc-42: cell division cycle 42.
Figure 4
Figure 4
Epigenetic effect of demethoxycurcumin and bisdemethoxycurcumin on lung cancer cells. WIF 1: Wnt Inhibitory Factor-1.
Figure 5
Figure 5
Modulation of microRNA by curcumin against lung cancer cells. The green arrow indicates upregulation, while the red arrow indicates downregulation of molecular targets and microRNAs. EZH2: enhancer of zeste homolog 2; Notch-1: neurogenic locus notch homolog protein-1; PTEN: phosphatase and tensin homolog; XIAP: X-linked inhibitor of apoptosis protein; PI3K: phosphatidylinositol 3-kinase; Akt: protein kinase; MMP-2: matrix metalloproteinase-2.

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