Autophagy: novel applications of nonsteroidal anti‐inflammatory drugs for primary cancer

Chen, Yu; Li, Weibing; Liu, Junbao; Lu, Jianwei; Feng, Jifeng

doi:10.1002/cam4.1287

Cited by 57 publications

(40 citation statements)

References 92 publications

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“…Numerous studies have indicated that autophagy can be mediated by various pathways, including PI3K/AKT/mTOR, AMPK/mTOR, MAPK/ERK1/2, P53/DRAM and HGF/MET . Among these pathways, the AMPK/mTOR signaling pathway plays a vital role in the process of autophagy.…”

Section: Resultsmentioning

confidence: 99%

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Thymoquinone inhibits the metastasis of renal cell cancer cells by inducing autophagy via AMPK/mTOR signaling pathway

et al. 2018

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Thymoquinone (TQ, 2‐methyl‐5‐isopropyl‐1,4‐benzoquinone), a bioactive constituent extracted from the seeds of Nigella sativa, has been proved to exert anti‐tumor efficiency in various cancers. Autophagy is a self‐digestion phenomenon, and its role in tumor formation and progression remains controversial. In the present study, we investigated the effects of TQ on renal cell cancer (RCC) cell lines (786‐O and ACHN) using wound healing assay, transwell assay and western blot analysis. We found that TQ effectively inhibited the metastatic capacity of RCC cells in vitro, which was also verified in a xenograft model. Meanwhile, we observed LC3 puncta and detected the expression of LC3 in TQ‐treated RCC cells, and then found that autophagy was induced by TQ in 786‐O and ACHN cell lines. In addition, TQ inhibited the migration and invasion as well as the EMT in RCC cells in an autophagy‐dependent manner. To further explore the underlying mechanism, we detected the AMPK/mTOR signaling pathway. The results indicated that TQ inhibited the metastasis of RCC cells by inducing autophagy via AMPK/mTOR signaling pathway. In conclusion, our findings provide a novel therapeutic strategy that aims at TQ‐induced autophagy in RCC treatment.

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Section: Resultsmentioning

confidence: 99%

“…AMPK is a cellular energy sensor that regulates homeostatic balance. It positively regulates autophagy by inhibiting the activity of mTORC1 through direct phosphorylation of its receptor, a regulatory‐associated protein of mTOR …”

Section: Discussionmentioning

confidence: 99%

Thymoquinone inhibits the metastasis of renal cell cancer cells by inducing autophagy via AMPK/mTOR signaling pathway

et al. 2018

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“…We, therefore, believe that CX-PC-casein-NPs show potential as a formulation for the intravenous administration of CX to treat cancer, since PC and caseins are safe for patients. CX is commercially used in many countries and is commonly administered two or three times (200 mg/time) a day to treat arthritis, menstrual pain, and chronic pain [29]. However, it exhibits poor solubility and variable absorption, which can lead to severe toxicity [14].…”

Section: The Inhibition Effect Of Cx-pc-casein-nps On Tumor Growthmentioning

confidence: 99%

Structural Modification of Nanomicelles through Phosphatidylcholine: The Enhanced Drug-Loading Capacity and Anticancer Activity of Celecoxib-Casein Nanoparticles for the Intravenous Delivery of Celecoxib

Qian

Wang

et al. 2020

Nanomaterials

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This study aims to stabilize loaded celecoxib (CX) by modifying the structure of casein nanoparticles through phosphatidylcholine. The results show that Egg yolk phosphatidylcholine PC98T (PC) significantly increased the stability of CX-PC-casein nanoparticles (NPs) (192.6 nm) from 5 min (CX-β-casein-NPs) to 2.5 h at 37 °C. In addition, the resuspended freeze-dried NPs (202.4 nm) remained stable for 2.5 h. Scanning electron microscopy indicated that PC may block the micropore structures in nanoparticles by ultrasonic treatment and hence improve the physicochemical stability of CX-PC-casein-NPs. The stability of the NPs was positively correlated with their inhibiting ability for human malignant melanoma A375 cells. The structural modification of CX-PC-casein-NPs resulted in an increased intracellular uptake of CX by 2.4 times than that of the unmodified ones. The pharmacokinetic study showed that the Area Under Curve (AUC) of the CX-PC-casein-NPs was 2.9-fold higher in rats than that of the original casein nanoparticles. When CX-PC-casein-NPs were intravenously administrated to mice implanted with A375 tumors (CX dose = 16 mg/kg bodyweight), the tumor inhibition rate reached 56.2%, which was comparable to that of paclitaxel (57.3%) at a dose of 4 mg/kg bodyweight. Our results confirm that the structural modification of CX-PC-casein-NPs can effectively prolong the remaining time of specific drugs, and may provide a potential strategy for cancer treatment.

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“…The inhibition of mTOR phosphorylation mediated by AMPK phosphorylation can induce autophagy in many different cell types. 15,16 Metformin is a widely used antidiabetic drug used to treat patients with type 2 diabetes mellitus. Studies have shown that it can exert protective effects against cardiovascular diseases; specifically, metformin can activate autophagy and provide cardioprotective effects in δ-sarcoglycan-deficient hearts.…”

Section: Introductionmentioning

confidence: 99%

<p>Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA <em>TUG1</em> to Induce Autophagy and Inhibit Atherosclerosis</p>

You¹,

Long²,

Song³

et al. 2020

DDDT

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Background: Metformin has been shown to inhibit the proliferation and migration of vascular wall cells. However, the mechanism through which metformin acts on atherosclerosis (AS) via the long non-coding RNA taurine up-regulated gene 1 (lncRNA TUG1) is still unknown. Thus, this research investigated the effect of metformin and lncRNA TUG1 on AS. Methods: First, qRT-PCR was used to detect the expression of lncRNA TUG1 in patients with coronary heart disease (CHD). Then, the correlation between metformin and TUG1 expression in vitro and their effects on proliferation, migration, and autophagy in vascular wall cells were examined. Furthermore, in vivo experiments were performed to verify the anti-AS effect of metformin and TUG1 to provide a new strategy for the prevention and treatment of AS. Results: qRT-PCR results suggested that lncRNA TUG1 expression was robustly upregulated in patients with CHD. In vitro experiments indicated that after metformin administration, the expression of lncRNA TUG1 decreased in a time-dependent manner. Metformin and TUG1 knockdown via small interfering RNA both inhibited proliferation and migration while promoted autophagy via the AMPK/mTOR pathway in vascular wall cells. In vivo experiments with a rat AS model further demonstrated that metformin and sh-TUG1 could inhibit the progression of AS. Conclusion: Taken together, our data demonstrate that metformin might function to prevent AS by activating the AMPK/mTOR pathway via lncRNA TUG1.

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Autophagy: novel applications of nonsteroidal anti‐inflammatory drugs for primary cancer

Cited by 57 publications

References 92 publications

Thymoquinone inhibits the metastasis of renal cell cancer cells by inducing autophagy via AMPK/mTOR signaling pathway

Thymoquinone inhibits the metastasis of renal cell cancer cells by inducing autophagy via AMPK/mTOR signaling pathway

Structural Modification of Nanomicelles through Phosphatidylcholine: The Enhanced Drug-Loading Capacity and Anticancer Activity of Celecoxib-Casein Nanoparticles for the Intravenous Delivery of Celecoxib

<p>Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA <em>TUG1</em> to Induce Autophagy and Inhibit Atherosclerosis</p>

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