Nicotine-induced survival signaling in lung cancer cells is dependent on their p53 status while its down-regulation by curcumin is independent

Puliyappadamba, Vineshkumar Thidil; Cheriyan, Vino T.; Thulasidasan, Arun Kumar T.; Bava, Smitha V.; Vinod, B.; Prabhu, Priya R.; Varghese, Ranji; Bevin, Arathy; Venugopal, Shalini; Anto, Ruby John

doi:10.1186/1476-4598-9-220

Cited by 49 publications

(38 citation statements)

References 61 publications

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“…We have reported that baicalin attenuates pulmonary inflammation by inhibiting NF-κB activation in cigarette smoke-induced COPD rat model (24). In the present study, expression of NF-κB p65 induced by nicotine in A549 cells differed from that in H1299 cells, depending on their p53 status (35). Flavones in Scutellaria dramatically downregulated NF-κB p65 protein expression in both cell types and elevated IκB-α protein expression in H1299 cells.…”

Section: Discussionmentioning

confidence: 44%

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Gong

Liu

et al. 2014

International Journal of Oncology

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Abstract. The objective of the present study was to investigate the therapeutic efficacy of flavonoid components in Scutellaria baicalensis on proliferation, metastasis and lung cancer-associated inflammation during nicotine induction in the A549 and H1299 lung cancer cell lines. After experimental period, augmentation of proliferation was observed, accompanied by marked decrease in apoptotic cells in nicotine-induced lung cancer cells; additionally, nicotine-exposed cells exhibited increased invasive and migratory abilities based on invasion and wound-healing assay. Flavones in Scutellaria, baicalin, baicalein and wogonin significantly counteracted the above deleterious changes. Moreover, assessment of tumor apoptotic and metastatic factors on mRNA levels by quantitative PCR and protein levels by western blotting revealed that these phytochemical treatments effectively negated nicotine-induced upregulated expression of bcl-2, bcl-2/bax ratio, caspase-3, matrix metalloproteinase (MMP)-2 and MMP-9 as well as downregulated expression of bax. Further analysis of inflammatory markers such as tumor necrosis factor (TNF)-α and interleukin (IL)-6 in cell culture supernatant and mRNA and protein expression of nuclear transcription factor-kappaB (NF-κB) and I kappa B-alpha (IκB-α) was carried out to substantiate the anti-inflammatory effect of flavones in Scutellaria in nicotine-exposed lung cancer cells. The therapeutic effects observed in the present study are attributed to the potent potential against proliferation, metastasis and inflammatory microenvironment by flavonoid components in Scutellaria in nicotine-induced lung cancer cells.

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Section: Discussionmentioning

confidence: 44%

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Gong

Liu

et al. 2014

International Journal of Oncology

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“…Some studies show that curcumin affects the expressin of cyclinD1, CDK4, CDK6 and p53, p21, p16 which are related to the regulation of cell cycle (Chen and Xu, 2005;Choudhuri et al, 2005;Divya and Pillai, 2006;Puliyappadamba et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Antifibrotic Effect of Curcumin in TGF-β1-Induced Myofibroblasts from Human Oral Mucosa

Zhang

Gong

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13, 289-294 IntroductionOral submucous fibrosis (OSF) is a chronic inflammatory disease, and has been defined by WHO as one of the precancerous conditions (International Agency for Research on Cancer, 2005). The main clinical symptoms include the stiffness of oral mucosa, restriction of mouth opening, atrophy of tongue papillae, blisters, and intolerance to hot and spicy food. Malignant transformation rate in OSF is high, reaching 7-13% (Tilakaratne et al., 2006). The disease exhibits characteristic histological features of excessive collagen deposition in the lamina propria, following the epithelium becomes atrophic (Singh et al., 2010).OSF is closely associated with betel quid (BQ) chewing, a habit common in South and Southeast Asia, some parts of Africa, and among immigrants from these regions (Boucher and Mannan, 2002). An imbalance in collagen synthesis and degradation in oral mucosa is generally believed to be the main cause of OSF;The disease is considered a type of collagen metabolism disorder (Rajalalitha and Vali, 2005).Myofibroblasts are typically activated fibroblasts, although they can also be derived from other cell types, including epithelial and endothelial cells via epithelial/ endothelial mesenchymal transition (EMT/EndMT) process, as well as from the circulating fibroblast-like cells AbstractBackground: Myofibroblasts play an important role in the development of oral submucous fibrosis (OSF). In the current study, we investigate the effect of curcumin on growth and apoptosis of myofibroblasts derived from human oral mucosa. Methods: Myofibroblasts were generated by incubating fibroblasts, obtained from human oral mucosa, with transforming growth factor-β1 (TGF-β1). MTT, PI staining, and FACS assays were used to investigate curcumin's effect on proliferation and cell cycle of fibroblasts and myofibroblasts. Annexin V/PI binding and FACS assays were used to examine apoptosis of myofibroblasts, Western blotting to determine the levels of Bcl-2 and Bax, and enzyme-linked immunosorbant assay was employed to examine the levels of collagen type I and III in the supernatants of myofibroblasts. Results: Curcumin inhibits proliferation of fibroblasts and myofibroblasts; it also disturbs the cell cycle, induces apoptosis and decreases the generation of collagen type I and III in myofibroblasts, which are more sensitive to its effects than fibroblasts. Curcumin induces apoptosis in myofibroblasts by down-regulating the Bcl-2/ Bax ratio. Conclusion: Our results demonstrate the antifibrotic effect of curcumin in vitro. It may therefore be a candidate for the treatment of OSF.

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“…Overwhelmingly, mechanisms of action reported for the antitumor efficacy of curcumin in lung cancer cells are via mitochondrial-mediated cell death elicited by an increase in the Bax:B cell lymphoma-2 ratio or by an increase in intracellular reactive oxygen species (ROS) (Chanvorachote et al, 2009;Pongrakhananon et al, 2010;Saha et al, 2010;Wu et al, 2010;Wang et al, 2011Wang et al, , 2013bSahoo et al, 2012;Yang et al, 2012a,b;Liu et al, 2013;Xiao et al, 2013;Chen et al, 2014). Migration and invasive capacity of lung cancer cells may be further decreased by inhibition of matrix metalloprotease expression, decreased nuclear factor-kB, EGFR, Akt, signal transducer and activator of transcription 3, and Cdc42 signaling (Chen et al, 2004(Chen et al, , 2012Lee et al, 2005;Lin et al, 2009Lin et al, , 2012Puliyappadamba et al, 2010;Kaushik et al, 2012;Liu et al, 2013;Yamauchi et al, 2014;Zhou et al, 2013a;Li et al, 2014b). Although drug resistance in lung cancer is a primary cause for therapeutic failure, very few in vitro models of resistance have been used when investigating the potential of curcumin for tertiary interventional strategies.…”

Section: Models For Tertiary Lung Cancer Preventionmentioning

confidence: 99%

Translating Curcumin to the Clinic for Lung Cancer Prevention: Evaluation of the Preclinical Evidence for Its Utility in Primary, Secondary, and Tertiary Prevention Strategies

Howells

Mahale

Sale

et al. 2014

J Pharmacol Exp Ther

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Lung cancer is responsible for over one million deaths worldwide each year. Smoking cessation for lung cancer prevention remains key, but it is increasingly acknowledged that prevention strategies also need to focus on high-risk groups, including ex-smokers, and patients who have undergone resection of a primary tumor. Models for chemoprevention of lung cancer often present conflicting results, making rational design of lung cancer chemoprevention trials challenging. There has been much focus on use of dietary bioactive compounds in lung cancer prevention strategies, primarily due to their favorable toxicity profile and long history of use within the human populace. One such compound is curcumin, derived from the spice turmeric. This review summarizes and stratifies preclinical evidence for chemopreventive efficacy of curcumin in models of lung cancer, and adjudges the weight of evidence for use of curcumin in lung cancer chemoprevention strategies.

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Nicotine-induced survival signaling in lung cancer cells is dependent on their p53 status while its down-regulation by curcumin is independent

Cited by 49 publications

References 61 publications

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Antifibrotic Effect of Curcumin in TGF-β1-Induced Myofibroblasts from Human Oral Mucosa

Translating Curcumin to the Clinic for Lung Cancer Prevention: Evaluation of the Preclinical Evidence for Its Utility in Primary, Secondary, and Tertiary Prevention Strategies

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