scholarly journals Salinomycin induces autophagic cell death in salinomycin-sensitive melanoma cells through inhibition of autophagic flux

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yajing Liu ◽  
Yinghua Hao ◽  
Yuxia Li ◽  
Yadan Zheng ◽  
Jiajing Dai ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Mrna Level ◽  
Melanoma Cells ◽  
Autophagic Cell Death ◽  
Autophagic Flux ◽  
Anti Cancer ◽  
Sensitive Line ◽  
Cancer Types ◽  
Insight Into

Abstract Several literature has shown that salinomycin (Sal) is able to kill various types of cancer cells through different signaling pathways. However, its effect on melanoma has seldom been reported. We examined the anti-cancer efficacy of Sal in melanoma cell lines, and found six of eight cell lines were sensitive to Sal. Given the fact that the roles of Sal are diverse in different cancer types, we were eager to figure out the mechanism involved in the current study. We noticed the most sensitive line, SK-Mel-19, showed a typical morphological change after Sal treatment. The autophagy inhibitor, 3-MA, could effectively suppress Sal-induced cell death. It could also facilitate the increase of autophagic markers and reduce the turnover of autophagosomes, which resulted in an aberrant autophagic flux. On the other hand, Sal could stimulate endoplasmic reticulum stress and cause an accumulation of dysfunctional mitochondria. We also discovered a potential correlation between LC3B mRNA level and its sensitivity to Sal in 43 clinical melanoma samples. Overall, our results indicated that Sal could have multiple effect on melanoma cells and induce autophagic cell death in certain kinds of cells, which provided a new insight into the chemotherapy for melanoma.

scholarly journals Selective Anti-Cancer Effects of Plasma-Activated Medium and Its High Efficacy with Cisplatin on Hepatocellular Carcinoma with Cancer Stem Cell Characteristics

2021 ◽  
Vol 22 (8) ◽  
pp. 3956
Author(s):  
Yan Li ◽  
Tianyu Tang ◽  
Hae June Lee ◽  
Kiwon Song
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Cell Lines ◽  
Primary Liver Cancer ◽  
Atmospheric Pressure Plasma ◽  
Normal Liver ◽  
Normal Liver Cell ◽  
Ample Evidence ◽  
Huh7 Cells ◽  
Anti Cancer

Hepatocellular carcinoma (HCC) is a major histological subtype of primary liver cancer. Ample evidence suggests that the pathological properties of HCC originate from hepatic cancer stem cells (CSCs), which are responsible for carcinogenesis, recurrence, and drug resistance. Cold atmospheric-pressure plasma (CAP) and plasma-activated medium (PAM) induce apoptosis in cancer cells and represent novel and powerful anti-cancer agents. This study aimed to determine the anti-cancer effect of CAP and PAM in HCC cell lines with CSC characteristics. We showed that the air-based CAP and PAM selectively induced cell death in Hep3B and Huh7 cells with CSC characteristics, but not in the normal liver cell line, MIHA. We observed both caspase-dependent and -independent cell death in the PAM-treated HCC cell lines. Moreover, we determined whether combinatorial PAM therapy with various anti-cancer agents have an additive effect on cell death in Huh7. We found that PAM highly increased the efficacy of the chemotherapeutic agent, cisplatin, while enhanced the anti-cancer effect of doxorubicin and the targeted-therapy drugs, trametinib and sorafenib to a lesser extent. These findings support the application of CAP and PAM as anti-cancer agents to induce selective cell death in cancers containing CSCs, suggesting that the combinatorial use of PAM and some specific anti-cancer agents is complemented mechanistically.

scholarly journals The TLR7 agonist imiquimod induces anti-cancer effects via autophagic cell death and enhances anti-tumoral and systemic immunity during radiotherapy for melanoma

Oncotarget ◽  
2017 ◽  
Vol 8 (15) ◽  
pp. 24932-24948 ◽  
Author(s):  
Jeong Hyun Cho ◽  
Hyo-Ji Lee ◽  
Hyun-Jeong Ko ◽  
Byung-Il Yoon ◽  
Jongseon Choe ◽  
...  
Keyword(s):  
Cell Death ◽  
Autophagic Cell Death ◽  
Systemic Immunity ◽  
Tlr7 Agonist ◽  
Anti Cancer

scholarly journals The Comprehensive Roles of ATRANORIN, A Secondary Metabolite from the Antarctic Lichen Stereocaulon caespitosum, in HCC Tumorigenesis

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1414 ◽  
Author(s):  
Young-Jun Jeon ◽  
Sanghee Kim ◽  
Ji Hee Kim ◽  
Ui Joung Youn ◽  
Sung-Suk Suh
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Genetic Diseases ◽  
Annexin V ◽  
Cancer Therapeutics ◽  
Metastatic Potential ◽  
Anti Cancer ◽  
Experimental Approaches ◽  
The Antarctic ◽  
Death Determination

Hepatocellular carcinoma (HCC) is one of the most deadly genetic diseases, but surprisingly chemotherapeutic approaches against HCC are only limited to a few targets. In particular, considering the difficulty of a chemotherapeutic drug development in terms of cost and time enforces searching for surrogates to minimize effort and maximize efficiency in anti-cancer therapy. In spite of the report that approximately one thousand lichen-derived metabolites have been isolated, the knowledge about their functions and consequences in cancer development is relatively limited. Moreover, one of the major second metabolites from lichens, Atranorin has never been studied in HCC. Regarding this, we comprehensively analyze the effect of Atranorin by employing representative HCC cell lines and experimental approaches. Cell proliferation and cell cycle analysis using the compound consistently show the inhibitory effects of Atranorin. Moreover, cell death determination using Annexin-V and (Propidium Iodide) PI staining suggests that it induces cell death through necrosis. Lastly, the metastatic potential of HCC cell lines is significantly inhibited by the drug. Taken these together, we claim a novel functional finding that Atranorin comprehensively suppresses HCC tumorigenesis and metastatic potential, which could provide an important basis for anti-cancer therapeutics.

scholarly journals Autophagic Cell Death Is Induced by Acetone and Ethyl Acetate Extracts fromEupatorium odoratum In Vitro: Effects on MCF-7 and Vero Cell Lines

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Faizah Bt. Harun ◽  
Syed Mohsin Syed Sahil Jamalullail ◽  
Khoo Boon Yin ◽  
Zulkhairi Othman ◽  
Anita Tilwari ◽  
...  
Keyword(s):  
Cell Death ◽  
Ethyl Acetate ◽  
Cytotoxic Activity ◽  
Vero Cell ◽  
Cell Lines ◽  
Autophagic Cell Death ◽  
Biologically Active ◽  
Vero Cell Lines ◽  
Mcf 7 ◽  
Ethyl Acetate Extracts

Eupatorium odoratum (EO)contains many biologically active compounds, the anticancer effects of which are not well documented. This study evaluates the cytotoxic effects and mechanism of action ofEOextracts on MCF-7 and Vero cell lines. Evaluation of the cytotoxic activity using MTT assay, morphological alterations, and apoptosis were carried out. Autophagy was evaluated by LC3-A protein expression. Cytotoxic activity, membrane blebbing and ballooning at 24 hours, replacement by mass vacuolation, and double membrane vesicles mimicking autophagy and cell death were observed in the cancer cells. No apoptosis was observed by DNA fragmentation assay. Overexpression of LC3-A protein indicated autophagic cell death. Cell cycle analysis showed G0 and G2/M arrest. The Vero cells did not show significant cell death at concentrations <100 μg/mL. These results thus suggest that acetone and ethyl acetate extracts ofEOinduce cell death through induction of autophagy and hold potential for development as potential anticancer drugs.

Anti-cancer Applications of Titanocene-Functionalised Nanostructured Systems: An Insight into Cell Death Mechanisms

2014 ◽  
Vol 20 (34) ◽  
pp. 10811-10828 ◽  
Author(s):  
Jesús Ceballos-Torres ◽  
Piroska Virag ◽  
Mihai Cenariu ◽  
Sanjiv Prashar ◽  
Mariano Fajardo ◽  
...  
Keyword(s):  
Cell Death ◽  
Anti Cancer ◽  
Nanostructured Systems ◽  
Cell Death Mechanisms ◽  
Insight Into

scholarly journals Up-regulation of Arl4a gene expression by broccoli aqueous extract is associated with improved spermatogenesis in mouse testes

Biomédica ◽  
2021 ◽  
Vol 41 (4) ◽  
Author(s):  
Omid Jazayeri ◽  
Setareh Farahmand Araghi ◽  
Tahereh A. Aghajanzadeh ◽  
Fereshteh Mir Moammadrezaei
Keyword(s):  
Gene Expression ◽  
Aqueous Extract ◽  
Sperm Count ◽  
Mrna Level ◽  
Treated Group ◽  
Sperm Number ◽  
Infertile Men ◽  
Anti Cancer ◽  
Insight Into ◽  
Mouse Body Weight

Introduction: Broccoli (Brassica oleracea) is well recognized due to its properties as an anti-cancer, antioxidant and scavenging free radicals. However, its benefit in enhancing spermatogenesis is not well understood. Objectives: To investigate the effect of broccoli aqueous extract on sperm factors and also expression of the involving genes (Catsper1, Catsper2, Arl4a, Sox5 and Sox9) in sperm factors in mice. Material and methods: Male mice were divided randomly into six groups: (1) Control, (2) Cadmium (3 mg/kg mouse body weight), (3) Orally treated with 200 broccoli aqueous extract (1 g ml-1), (4) Orally treated with 400 µl of broccoli aqueous extract, (5) Orally treated with 200 broccoli aqueous extract plus cadmium, and (6) Orally treated with 400 µl of broccoli aqueous extract plus cadmium. Sperms factors and also gene expression in Catsper1, Catsper2, Arl4a, Sox5 and Sox9 genes were studied. Results: An obvious improvement in sperm number and slight enhancement in sperm motility was observed in mice treated with broccoli extract with and without cadmium. While sperm viability was reduced by broccoli extract, except for 200 µl of broccoli extract with cadmium that was significantly increased. Interestingly, Arl4a gene expression showed an increase in 400 µl broccoli-treated group. Likewise, the Arl4a mRNA level in mice treated with cadmium along with 200 µl broccoli extract was higher than in cadmium-treated mice. Furthermore, broccoli extract enhanced the mRNA level of Catsper2 and Sox5 genes in mice treated with both 200 and 400 µl broccoli extract along with cadmium than the only cadmium-treated group. Conclusion: Generally, improvement in sperm count in broccoli-treated mice provides insight into the pharmaceutical industry to make new products available to infertile men.

scholarly journals Cell Death Induction Potential in Seed Extracts- Hidden and Bioactive Phytochemical Treasures

2021 ◽  
Vol 20 (4) ◽  
Author(s):  
R. Rajasekaran ◽  
P. K. Suresh
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Grape Seed ◽  
Seed Extract ◽  
Chemotherapeutic Drugs ◽  
Bioactive Components ◽  
Induce Cell Death ◽  
Grape Seed Proanthocyanidins ◽  
Anti Cancer ◽  
Seed Extracts

Seeds have been known to possess bioactive components with anti-cancer properties. This study aims to demonstrate the processes by which seed extracts from various sources induce cell death. Several assays have been employed to demonstrate the induction of cell death by the respective seed extracts. This review also underscores the importance of Grape Seed Proanthocyanidins (GSPs) in terms of inducing the aforesaid physiological form of seed extract-induced cell death. Furthermore, this review highlights the critical and pressing need to conduct comparative HTS-based strategies (with a battery of cell lines representing different cancers) to identify the major seed extracts that can reproducibly serve to augment the cell death induction capabilities of the existing battery of chemotherapeutic drugs/natural alternatives.

scholarly journals Apigenin Induces Autophagy and Cell Death by Targeting EZH2 under Hypoxia Conditions in Gastric Cancer Cells

2021 ◽  
Vol 22 (24) ◽  
pp. 13455
Author(s):  
Tae Woo Kim ◽  
Hee Gu Lee
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Er Stress ◽  
Fruits And Vegetables ◽  
Molecular Mechanisms ◽  
Autophagic Cell Death ◽  
Gastric Cancer Cells ◽  
Er Stress Response ◽  
Anti Cancer ◽  
Cancer Agent

Hypoxia is a major obstacle to gastric cancer (GC) therapy and leads to chemoresistance as GC cells are frequently exposed to the hypoxia environment. Apigenin, a flavonoid found in traditional medicine, fruits, and vegetables and an HDAC inhibitor, is a powerful anti-cancer agent against various cancer cell lines. However, detailed mechanisms involved in the treatment of GC using APG are not fully understood. In this study, we investigated the biological activity of and molecular mechanisms involved in APG-mediated treatment of GC under hypoxia. APG promoted autophagic cell death by increasing ATG5, LC3-II, and phosphorylation of AMPK and ULK1 and down-regulating p-mTOR and p62 in GC. Furthermore, our results show that APG induces autophagic cell death via the activation of the PERK signaling, indicating an endoplasmic reticulum (ER) stress response. The inhibition of ER stress suppressed APG-induced autophagy and conferred prolonged cell survival, indicating autophagic cell death. We further show that APG induces ER stress- and autophagy-related cell death through the inhibition of HIF-1α and Ezh2 under normoxia and hypoxia. Taken together, our findings indicate that APG activates autophagic cell death by inhibiting HIF-1α and Ezh2 under hypoxia conditions in GC cells.

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