Autophagy-associated Targeting Pathways of Natural Products during Cancer Treatment

Zhang, Shufang; Wang, Xiaolu; Yang, Xiaoqi; Chen, Ning

doi:10.7314/apjcp.2014.15.24.10557

Cited by 39 publications

(45 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, autophagy may play an oncogenic role by maintaining tumor cell survival and preventing apoptotic cell death after anticancer treatment. Recently, several studies demonstrated that natural compounds with anticancer abilities could induce autophagy in different types of tumors (20)(21)(22). However, the precise role of autophagy (tumor suppressor or promoter) involved in the mechanism of natural compound-induced cancer cell death needs to be further studied.…”

Section: Introductionmentioning

confidence: 99%

Curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells

Zhou

Yang

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

Abstract. Curcumin possesses an anticancer effect against a wide assortment of tumors with selective cytotoxicity for tumor cells. However, the mechanism involved in the curcumin-induced anticancer effect remain unclear. In the present study, we investigated the efficacy of curcumin against human gastric cancer cell growth and the molecular mechanism involved. Our results demonstrated that curcumin inhibited the viabilities of gastric cancer cell lines BGC-823, SGC-7901 and MKN-28 in both a time-and dose-dependent manner. In addition, curcumin treatment induced gastric cancer cell apoptosis in a dose-responsive manner. Western blotting of apoptosis-related proteins further confirmed the pro-apoptotic potential of curcumin. After exposure to curcumin, a robust induction of autophagy was observed in gastric cancer cells, which was characterized by the formation of acidic vesicular organelles (AVOs), conversion of LC3-I to LC3-II and an increase in the levels of autophagy-related proteins. Activation of the PI3K/Akt/mTOR signaling pathway was suppressed in gastric cancer cells with curcumin treatment. However, administration of the autophagy inhibitor 3-methyladenine (3-MA) significantly promoted the apoptotic cell death induced by curcumin. Collectively, our findings provide new evidence that curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells in vitro. Autophagy inhibitor treatment may provide a novel and effective strategy for improving the anticancer effect of curcumin against gastric cancer.

show abstract

Section: Introductionmentioning

confidence: 99%

Curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells

Zhou

Yang

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…Up to date various pathways underlying the programmed cell death include apoptosis, autophagy, and necroptosis, as reviewed elsewhere [18-23]. While numerous reviews focused on the apoptotic pathways, extrinsic and intrinsic alike, we concentrate our efforts on the latest developments regarding autophagy and necroptosis induced by natural compounds in tumor cells [24-29]. Apoptosis is the most often occurred mechanism of tumor cell death induced upon chemotherapeutic treatment.…”

Section: Introductionmentioning

confidence: 99%

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

Guamán-Ortiz

Orellana²,

Ratovitski³

2017

View full text Add to dashboard Cite

Cell death is an innate capability of cells to be removed from microenvironment, if and when they are damaged by multiple stresses. Cell death is often regulated by multiple molecular pathways and mechanism, including apoptosis, autophagy, and necroptosis. The molecular network underlying these processes is often intertwined and one pathway can dynamically shift to another one acquiring certain protein components, in particular upon treatment with various drugs. The strategy to treat human cancer ultimately relies on the ability of anticancer therapeutics to induce tumor-specific cell death, while leaving normal adjacent cells undamaged. However, tumor cells often develop the resistance to the drug-induced cell death, thus representing a great challenge for the anticancer approaches. Numerous compounds originated from the natural sources and biopharmaceutical industries are applied today in clinics showing advantageous results. However, some exhibit serious toxic side effects. Thus, novel effective therapeutic approaches in treating cancers are continued to be developed. Natural compounds with anticancer activity have gained a great interest among researchers and clinicians alike since they have shown more favorable safety and efficacy then the synthetic marketed drugs. Numerous studies in vitro and in vivo have found that several natural compounds display promising anticancer potentials. This review underlines certain information regarding the role of natural compounds from plants, microorganisms and sea life forms, which are able to induce non-apoptotic cell death in tumor cells, namely autophagy and necroptosis.

show abstract

“…Thus, its function as an active cell death mechanism remains controversial [1]. Actually, most reported autophagy induced by natural products was prosurvival [6, 7]. Regulated necrosis is morphologically characterized by cytoplasmic granulation, organelle and/or cellular swelling resulting from cellular leakage [8].…”

Section: Introductionmentioning

confidence: 99%

PTEN Activation by DNA Damage Induces Protective Autophagy in Response to Cucurbitacin B in Hepatocellular Carcinoma Cells

Niu

Sun

et al. 2016

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Cucurbitacin B (Cuc B), a natural product, induced both protective autophagy and DNA damage mediated by ROS while the detailed mechanisms remain unclear. This study explored the mechanism of Cuc B-induced DNA damage and autophagy. Cuc B decreased cell viability in concentration- and time-dependent manners. Cuc B caused long comet tails and increased expression of γ-H2AX, phosphorylation of ATM/ATR, and Chk1/Chk2. Cuc B induced autophagy as evidenced by monodansylcadaverine (MDC) staining, increased expression of LC3II, phosphorylated ULK1, and decreased expression of phosphorylated AKT, mTOR. Cuc B induced apoptosis mediated by Bcl-2 family proteins and caspase activation. Furthermore, Cuc B induced ROS formation, which was inhibited by N-acetyl-L-cysteine (NAC). NAC pretreatment dramatically reversed Cuc B-induced DNA damage, autophagy, and apoptosis. Cuc B-induced apoptosis was reversed by NAC but enhanced by 3-methyladenine (3-MA), chloroquine (CQ), and silencing phosphatase and tensin homolog (PTEN). 3-MA and CQ showed no effect on Cuc B-induced DNA damage. In addition, Cuc B increased PTEN phosphorylation and silence PTEN restored Cuc B-induced autophagic protein expressions without affecting DNA damage. In summary, Cuc B induced DNA damage, apoptosis, and protective autophagy mediated by ROS. PTEN activation in response to DNA damage bridged DNA damage and prosurvival autophagy.

show abstract

Autophagy-associated Targeting Pathways of Natural Products during Cancer Treatment

Cited by 39 publications

References 80 publications

Curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells

Curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

PTEN Activation by DNA Damage Induces Protective Autophagy in Response to Cucurbitacin B in Hepatocellular Carcinoma Cells

Contact Info

Product

Resources

About