Curcumin inhibits the development of non‑small cell lung cancer by inhibiting autophagy and apoptosis

Wang, Aili; Wang, Jinxiang; Zhang, Shuming; Zhang, Hongxia; Xu, Zhiyun; Li, Xiaohui

doi:10.3892/etm.2017.5172

Cited by 28 publications

(23 citation statements)

References 28 publications

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“…It has been reported to exhibit extensive pharmacological activity, with anti-inflammatory, antioxidative, and antitumor properties. In recent years, several studies have investigated the antifibrotic effects of curcumin on organs such as the liver and kidney [11, 26–29]. However, thus far, no accounts of curcumin use for joint contracture have been reported.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Inhibits Joint Contracture through PTEN Demethylation and Targeting PI3K/Akt/mTOR Pathway in Myofibroblasts from Human Joint Capsule

Zhuang

Chen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Joint contracture is increasingly regarded as a clinical problem that leads to irreversible dysfunction of the joint. It is a pathophysiological process following joint injury, which is marked by the activation of myofibroblasts. There is currently no effective treatment for the prevention of joint contracture. Curcumin is a polyphenol pigment extracted from turmeric, which possesses anti-inflammatory, antioxidative, and antitumor properties. In the present study, we demonstrated that curcumin exerts a protective effect against joint contracture via the inhibition of myofibroblast proliferation and migration in a time- and concentration-dependent manner. Moreover, we indicated that phosphatase and tension homolog (PTEN) was downregulated in myofibroblasts in vitro and in the contracture capsule tissues of patients in vivo. Additionally, western blot analysis revealed a negative correlation between the expression levels of PTEN and the fibrosis marker protein alpha smooth muscle cell actin. Methylation-specific PCR results suggested that curcumin was able to demethylate PTEN in a similar manner to the demethylation agent 5-azacytidine, increasing PTEN expression and further inhibiting phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling. In conclusion, our data illustrate part of the mechanism of curcumin inhibition in joint contracture. These results support the hypothesis that curcumin may potentially be used as a novel candidate for the treatment of joint contracture.

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Section: Discussionmentioning

confidence: 99%

Curcumin Inhibits Joint Contracture through PTEN Demethylation and Targeting PI3K/Akt/mTOR Pathway in Myofibroblasts from Human Joint Capsule

Zhuang

Chen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Section: Phosphatidylinositol-3-kinase-akt-mtor (Pi3k/akt/mtor)mentioning

confidence: 90%

“…Curcumin was shown to inhibit PI3K/Akt/mTOR pathways in NSCLC cells A549 [118] and H1299 [119]. The findings demonstrated that curcumin treatment suppresses the PI3K/Akt/mTOR pathway by decreasing the Akt and mTOR phosphorylation thus inducing apoptosis [119,120]. On a different note, a tumor suppressor phosphatase and tensin homolog (PTEN) protein has been found to inactivate PI3K/Akt/mTOR pathways through dephosphorylation of PIP 3 to PIP 2 [121].…”

Section: Phosphatidylinositol-3-kinase-akt-mtor (Pi3k/akt/mtor)mentioning

confidence: 98%

Mechanistic Understanding of Curcumin’s Therapeutic Effects in Lung Cancer

et al. 2019

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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.

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“…Further investigations confirmed that curcumin (40 µM) triggered autophagy in A549 cells through the activation of the AMPK signaling pathway, an increase in gene expression levels of human ganglioside (GD)-3 synthase (hST8Sia I) and of its catalyzed protein product GD [ 206 ]. Similarly, Wang et al reported that curcumin (10 µM) inhibited the growth of other NSCLC cells (H1299; A549), it suppressed PI3K/Akt/mTOR activation and thus it induced apoptosis and autophagy [ 207 ]. Moreover, curcumin (15 µM) enhanced the autophagy induced by galbanic acid (40 µM), a sesquiterpene coumarin in NSCLC A549 cells.…”

Section: In Vitro- and In Vivo-mediated Autophagy By Polyphenolsmentioning

confidence: 99%

Polyphenol-Mediated Autophagy in Cancer: Evidence of In Vitro and In Vivo Studies

Benvenuto

Albonici

Focaccetti

et al. 2020

IJMS

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One of the hallmarks of cellular transformation is the altered mechanism of cell death. There are three main types of cell death, characterized by different morphological and biochemical features, namely apoptosis (type I), autophagic cell death (type II) and necrosis (type III). Autophagy, or self-eating, is a tightly regulated process involved in stress responses, and it is a lysosomal degradation process. The role of autophagy in cancer is controversial and has been associated with both the induction and the inhibition of tumor growth. Autophagy can exert tumor suppression through the degradation of oncogenic proteins, suppression of inflammation, chronic tissue damage and ultimately by preventing mutations and genetic instability. On the other hand, tumor cells activate autophagy for survival in cellular stress conditions. Thus, autophagy modulation could represent a promising therapeutic strategy for cancer. Several studies have shown that polyphenols, natural compounds found in foods and beverages of plant origin, can efficiently modulate autophagy in several types of cancer. In this review, we summarize the current knowledge on the effects of polyphenols on autophagy, highlighting the conceptual benefits or drawbacks and subtle cell-specific effects of polyphenols for envisioning future therapies employing polyphenols as chemoadjuvants.

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Curcumin inhibits the development of non‑small cell lung cancer by inhibiting autophagy and apoptosis

Cited by 28 publications

References 28 publications

Curcumin Inhibits Joint Contracture through PTEN Demethylation and Targeting PI3K/Akt/mTOR Pathway in Myofibroblasts from Human Joint Capsule

Curcumin Inhibits Joint Contracture through PTEN Demethylation and Targeting PI3K/Akt/mTOR Pathway in Myofibroblasts from Human Joint Capsule

Mechanistic Understanding of Curcumin’s Therapeutic Effects in Lung Cancer

Polyphenol-Mediated Autophagy in Cancer: Evidence of In Vitro and In Vivo Studies

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