Curcumin Modulates Paraquat-Induced Epithelial to Mesenchymal Transition by Regulating Transforming Growth Factor-β (TGF-β) in A549 Cells

Tyagi, Namitosh; Singh, Digvijay; Dash, Debabrata; Singh, Rashmi

doi:10.1007/s10753-019-01006-0

Cited by 18 publications

(10 citation statements)

References 37 publications

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“…Exposing lung cancer cells into paraquat (PQ) significantly increases their migration and invasion through TGF-β-induced EMT. The administration of curcumin inhibits TGF-β signaling to suppress EMT, leading to preserving E-cadherin and reducing cancer malignancy (Tyagi et al, 2019). Oxaliplatin (OX) is a chemotherapeutic agent for eliminating cancer cells and enhancing overall survival of patients with cancer (Li et al, 2020a).…”

Section: Cancermentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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Immune response, proliferation, migration and angiogenesis are juts a few of cellular events that are regulated by transforming growth factor-β (TGF-β) in cells. A number of studies have documented that TGF-β undergoes abnormal expression in different diseases, e.g., diabetes, cancer, fibrosis, asthma, arthritis, among others. This has led to great fascination into this signaling pathway and developing agents with modulatory impact on TGF-β. Curcumin, a natural-based compound, is obtained from rhizome and roots of turmeric plant. It has a number of pharmacological activities including antioxidant, anti-inflammatory, anti-tumor, anti-diabetes and so on. Noteworthy, it has been demonstrated that curcumin affects different molecular signaling pathways such as Wnt/β-catenin, Nrf2, AMPK, mitogen-activated protein kinase and so on. In the present review, we evaluate the potential of curcumin in regulation of TGF-β signaling pathway to corelate it with therapeutic impacts of curcumin. By modulation of TGF-β (both upregulation and down-regulation), curcumin ameliorates fibrosis, neurological disorders, liver disease, diabetes and asthma. Besides, curcumin targets TGF-β signaling pathway which is capable of suppressing proliferation of tumor cells and invading cancer cells.

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Section: Cancermentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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“…These findings were corroborated by the oncology array platform, which demonstrated that long-term, low-dose curcumin favours upregulation of anti-carcinogenic, and downregulation of pro-carcinogenic proteins, many of which are associated with epithelial to mesenchymal transition (EMT). Curcumin has previously been shown to play a role in preventing or reversing the generation of an EMT phenotype [16][17][18][19], albeit at single, non-pharmacologic high doses ranging from 10 to 80 µM. Such high doses are unlikely to be attained clinically, making it difficult to interpret and translate mechanistic relevance to prevention strategies that are typified by sub-micromolar systemic curcuminoid availability.…”

Section: Discussionmentioning

confidence: 99%

New Paradigms to Assess Consequences of Long-Term, Low-Dose Curcumin Exposure in Lung Cancer Cells

et al. 2020

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Curcumin has been investigated extensively for cancer prevention, but it has been proposed that long-term treatments may promote clonal evolution and gain of cellular resistance, potentially rendering cancer cells less sensitive to future therapeutic interventions. Here, we used long-term, low-dose treatments to determine the potential for adverse effects in non-small cell lung cancer (NSCLC) cells. IC50s for curcumin, cisplatin, and pemetrexed in A549, PC9, and PC9ER NSCLC cells were evaluated using growth curves. IC50s were subsequently re-assessed following long-term, low-dose curcumin treatment and a three-month treatment withdrawal period, with a concurrent assessment of oncology-related protein expression. Doublet cisplatin/pemetrexed-resistant cell lines were created and the IC50 for curcumin was determined. Organotypic NSCLC-fibroblast co-culture models were used to assess the effects of curcumin on invasive capacity. Following long-term treatment/treatment withdrawal, there was no significant change in IC50s for the chemotherapy drugs, with chemotherapy-resistant cell lines exhibiting similar sensitivity to curcumin as their non-resistant counterparts. Curcumin (0.25–0.5 µM) was able to inhibit the invasion of both native and chemo-resistant NSCLC cells in the organotypic co-culture model. In summary, long-term curcumin treatment in models of NSCLC neither resulted in the acquisition of pro-carcinogenic phenotypes nor caused resistance to chemotherapy agents.

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“…Curcumin's effects on the tumour microenvironment also include activation of the immune system and suppression of angiogenesis and chemoresistance and immune resistance. Akt, protein kinase B; Bcl-2, B cell lymphoma 2; CAF, cancer-associated fibroblast; COX-2, cyclooxygenase-2; EGF, endothelial growth factor; [128,196,[242][243][244][245]248,249,276,[279][280][281][282][283][284]. NSCLC is associated with dysregulation of numerous signalling and regulatory pathways.…”

Section: Effect Of Curcumin and Flavonoids On The Migration Of Cancer Cellsmentioning

confidence: 99%

“…Figure 4. Simplified model of the effects of curcumin on NSCLC cells[128,196,[242][243][244][245]248,249,276,[279][280][281][282][283][284]. NSCLC…”

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confidence: 99%

Circulating Tumour Cells (CTCs) in NSCLC: From Prognosis to Therapy Design

et al. 2021

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Designing optimal (neo)adjuvant therapy is a crucial aspect of the treatment of non-small-cell lung carcinoma (NSCLC). Standard methods of chemotherapy, radiotherapy, and immunotherapy represent effective strategies for treatment. However, in some cases with high metastatic activity and high levels of circulating tumour cells (CTCs), the efficacy of standard treatment methods is insufficient and results in treatment failure and reduced patient survival. CTCs are seen not only as an isolated phenomenon but also a key inherent part of the formation of metastasis and a key factor in cancer death. This review discusses the impact of NSCLC therapy strategies based on a meta-analysis of clinical studies. In addition, possible therapeutic strategies for repression when standard methods fail, such as the administration of low-toxicity natural anticancer agents targeting these phenomena (curcumin and flavonoids), are also discussed. These strategies are presented in the context of key mechanisms of tumour biology with a strong influence on CTC spread and metastasis (mechanisms related to tumour-associated and -infiltrating cells, epithelial–mesenchymal transition, and migration of cancer cells).

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Curcumin Modulates Paraquat-Induced Epithelial to Mesenchymal Transition by Regulating Transforming Growth Factor-β (TGF-β) in A549 Cells

Cited by 18 publications

References 37 publications

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

New Paradigms to Assess Consequences of Long-Term, Low-Dose Curcumin Exposure in Lung Cancer Cells

Circulating Tumour Cells (CTCs) in NSCLC: From Prognosis to Therapy Design

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