The effects of curcumin on proliferation, apoptosis, invasion, and NEDD4 expression in pancreatic cancer

Su, Jingna; Zhou, Xiaodong; Yin, Xuyuan; Wang, Lixia; Zhao, Zhe; Hou, Yingying; Zheng, Nana; Xia, Jun; Wang, Zhiwei

doi:10.1016/j.bcp.2017.05.014

Cited by 42 publications

(28 citation statements)

References 32 publications

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“…cancer cell migration and invasion and suppressed NEDD4 expression (40). In our previous study, we also demonstrated that LY294002 exposure for 24 h reduced the migration of pancreatic cancer cells without the addition of SOD (41).…”

Section: Discussionsupporting

confidence: 57%

Curcumin inhibits superoxide dismutase-induced epithelial-to-mesenchymal transition via the PI3K/Akt/NF-κB pathway in pancreatic cancer cells

Jiang

Xiao

et al. 2018

Int J Oncol

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Curcumin is a natural polyphenol compound derived from turmeric. It possesses multiple pharmacological properties, including antioxidant, anti-inﬂammatory and anti-tumor progression properties. Our recent study demonstrated that superoxide dismutase (SOD)-dependent production of hydrogen peroxide (H2O2) promoted the invasive and migratory activity of pancreatic cancer cells. However, whether curcumin suppresses SOD-induced cancer progression and the related mechanisms remains unclear. Since epithelial‑to-mesenchymal transition (EMT) plays a key role in tumor metastasis, the aim of the present study was to examine whether curcumin intervenes with SOD-induced EMT in pancreatic cancer and the underlying mechanism. The human pancreatic cancer cells BxPC-3 and Panc-1 were exposed to SOD in the presence or absence of curcumin, catalase (CAT, a scavenger of H2O2), or LY 294002 [a phosphoinositide-3 kinase (PI3K) inhibitor]. Intracellular reactive oxygen species (ROS) and H2O2 were evaluated by 2,7-dichlorodihydroﬂuorecein diacetate and H2O2 assay, respectively. The activation of p-Akt and p-nuclear factor (NF)-κB were examined by western blotting. The migratory and invasive abilities of pancreatic cancer cells were tested by the wound healing and Transwell invasion assays. The expression of E-cadherin, N-cadherin and vimentin (EMT-related genes) were measured by reverse transcription-quantitative polymerase chain reaction and western blotting at the mRNA and protein levels, respectively. The findings of the present study demonstrated that curcumin decreased SOD-induced production of ROS and H2O2 in BxPC-3 and Panc-1 cells. Curcumin was able to suppress SOD-induced invasion and migration, and it also regulated the expression of the above‑mentioned EMT-related genes and cell morphology. SOD-induced cell invasion was also inhibited by catalase and LY 294002. Furthermore, the levels of p-Akt and p-NF-κB caused by SOD could be offset by treatment with curcumin and LY 294002. To summarize, these results demonstrated that curcumin was able to prevent SOD-driven H2O2-induced pancreatic cancer metastasis by blocking the PI3K/Akt/NF-κB signaling pathway. The use of curcumin to inhibit the H2O2/Akt/NF-κB axis may be a promising therapeutic approach to the treatment of patients with pancreatic cancer.

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Section: Discussionsupporting

confidence: 57%

Curcumin inhibits superoxide dismutase-induced epithelial-to-mesenchymal transition via the PI3K/Akt/NF-κB pathway in pancreatic cancer cells

Jiang

Xiao

et al. 2018

Int J Oncol

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“…NEDD4 was also identified to regulate a large number of molecules that modulate signaling pathways to control cell growth and cancer development [19,38]. It was reported that NEDD4 is frequently overexpressed in many types of human cancers and always negatively regulate tumor suppressor PTEN [18,24,[39][40][41]. One study showed that depletion of NEDD4 inhibited cell proliferation in bladder cancer cells [42].…”

Section: Discussionmentioning

confidence: 99%

“…Amodio et al demonstrated that NEDD4 facilitated non-smallcell lung carcinomas (NSCLC) cell lines proliferation through inactivation of PTEN [22]. Recently, curcumin was identified to exert its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma and pancreatic cancer cells [23,24]. In hepatic cancer cells, NEDD4 was reported to associate with low density lipoprotein receptor class A domain containing 4 (LDLRAD4) and exhibited an oncogenic role in tumorigenesis [25].…”

Section: Introductionsmentioning

confidence: 99%

NEDD4 promotes cell growth and motility in hepatocellular carcinoma

Zheng

et al. 2018

Cell Cycle

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Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death worldwide. In China, the situation is even worse as cancer incidence and mortality continue to increase rapidly. Although tremendous progress has been made toward HCC treatments, the benefits for liver cancer patients are still limited. Therefore, it is necessary to identify and develop novel therapeutic methods. Neuronally expressed developmentally downregulated 4 (NEDD4), an E3 ubiquitin ligase, plays a critical role in the development and progression of various types of human cancers. In our study, NEDD4 acts as an oncoprotein in both QGY7703 and SMMC7721 liver cancer cell lines. We found that depletion of NEDD4 by siRNA transfection led to inhibition of cell growth, invasion and migration, and promotion of apoptosis. In contrast, overexpression of NEDD4 via plasmid transfection resulted in facilitated cell proliferation, invasion and migration, and decreased apoptosis. Importantly, we observed that tumor suppressor LATS1, also a core component of Hippo pathway, was negatively regulated by NEDD4 in liver cancer cells. Our findings suggested that NEDD4 may be involved in the HCC progression via regulating LATS1 associated signaling pathway. Therefore, targeting NEDD4-LATS1 signaling could be a potential therapeutic option for HCC treatment.

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“…Improvements in its treatment are essential. 2,3 Numerous attempts have been made by researchers to find new anticancer drugs of natural origin such as thymoquinone, 4 curcumin, 5 and papaverine. 6 3, 3′diindolylmethane (DIM), which has been isolated from broccoli, Brussels sprouts, cabbage, and kale and ellagic acid (EA), which is present in raspberries and blackberries, have anticancer properties, but they are insoluble or unstable.…”

Section: Introductionmentioning

confidence: 99%

<p>Nanoformulated Bioactive Compounds Derived from Different Natural Products Combat Pancreatic Cancer Cell Proliferation</p>

Mousa¹,

El‐Far²,

Saddiq³

et al. 2020

IJN

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This study was designed to determine the potential effect of nanoencapsulated bioactive compounds from different natural sources on human pancreatic cancer. Background: Pancreatic cancer carries the highest fatality rate among all human cancers because of its high metastatic potential and late presentation at the time of diagnosis. Hence there is a need for improved methods to prevent and treat it. Natural products, such as 3, 3′diindolylmethane (DIM) and ellagic acid (EA) demonstrated anticancer efficacy against various cancer types. However, DIM is insoluble. Hence, using nanotechnology to encapsulate these compounds in combination with EA might improve their physical and chemical properties and their delivery to the cancer cells. Methods: Human pancreatic cancer cells, namely SUIT2-luciferase transfected, were used to examine the effects of DIM or EA and their nanoformulation in poly(lactic-co-glycolic acid) (PLGA) and poly(ethylene glycol) (PEG) [PLGA-PEG] nanoparticles (NPs) on SUIT2luciferase cell viability/proliferation over 24 hrs. Additionally, effects on tumor weight and angiogenesis were determined using the chick chorioallantoic membrane (CAM) tumor implant model. Results: Both DIM and EA PLGA-PEG NPs resulted in rapid suppression of pancreatic cancer cell viability/proliferation within 24 hrs (P < 0.01), while the non-encapsulated DIM and EA did not show any significant effect on SUIT2 cancer cell viability or cell proliferation (MTT assay). In the CAM pancreatic cancer cell (SUIT2) implant model, results showed a greater suppression of tumor weight (P < 0.01), tumor cell viability, and tumor angiogenesis (P < 0.01) for DIM NPs and EA NPs and their combinations versus DIM or EA alone. Conclusion: Nanoformulation of DIM and EA resulted in a more effective suppression of pancreatic cancer cell viability, pancreatic tumor weight, implanted cancer cell viability, and tumor angiogenesis as compared with these bioactive compounds alone.

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The effects of curcumin on proliferation, apoptosis, invasion, and NEDD4 expression in pancreatic cancer

Cited by 42 publications

References 32 publications

Curcumin inhibits superoxide dismutase-induced epithelial-to-mesenchymal transition via the PI3K/Akt/NF-κB pathway in pancreatic cancer cells

Curcumin inhibits superoxide dismutase-induced epithelial-to-mesenchymal transition via the PI3K/Akt/NF-κB pathway in pancreatic cancer cells

NEDD4 promotes cell growth and motility in hepatocellular carcinoma

<p>Nanoformulated Bioactive Compounds Derived from Different Natural Products Combat Pancreatic Cancer Cell Proliferation</p>

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