scholarly journals Correction to “The Novel Anti-Cancer Agent JNJ-26854165 Induces Cell Death through Inhibition of Cholesterol Transport and Degradation of ABCA1”

2013 ◽  
Vol 347 (2) ◽  
pp. 540-540
Keyword(s):  
Cell Death ◽  
Cholesterol Transport ◽  
The Novel ◽  
Anti Cancer ◽  
Cancer Agent

scholarly journals Berberine inhibits the proliferation of pancreatic cancer targeting pancreatic cancer stem cells

2021 ◽  
Author(s):  
Mengmeng Liu ◽  
Yue Pan ◽  
Xufeng Tao ◽  
Ning Li ◽  
Kun Li ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Clinical Effectiveness ◽  
The Novel ◽  
Migration Assay ◽  
Medicinal Value ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Pancreatic Cancer Stem Cells

Abstract BackgroundPDAC is universally acknowledged to be one of the highest mortality rate of cancer-related deaths. PCSCs, regulated by EMT, could promote the proliferation of PDAC. Berberine with high medicinal value has usually been used as an anti-cancer agent. Hence the purpose of this study is to investigate the anti-cancer effect of berberine in PDAC. MethodsMTT assay was used to verify berberine inhibiting the proliferation of PDAC. Immunofluorescence staining, stem cell sphere, wound healing and transwell migration assay were demonstrated the anti-proliferation and anti-stemness of PCSCs in vitro . PANC-02 cells were injected in C57BL/6 mice to establish the orthotopic pancreatic-cancer model in vivo . H&E and Ki67 immunohistogical staining assay were used to evaluated the effect of berberine in PDAC in vivo. q-PCR and Western blot methods were applied to detect the expression of EMT procedure.ResultsIn this study, berberine has selective anti-cancer effect in PDAC in vitro . Moreover, berberine suppressed the proliferation and stemness of PCSCs in PDAC. In vivo , berberine reduced the tumor size and decreased the expression of Ki67 in orthotopic pancreatic-cancer pancreases. In addition, berberine inhibit the EMT signaling pathway both in vitro and in vivo . ConclusionsOur study indicates that berberine inhibit the proliferation of PDAC in vivo and vitro . The mechanism of anti-cancer effect on berberine may suppress the PCSCs through inhibiting EMT procedure. Therefore, berberine may be the novel antineoplastic drug with clinical effectiveness in PDAC. Keywords: Berberine, PDAC, PCSCs, EMT, berberine

Chemical and enzymatic stability of a cyclic depsipeptide, the novel, marine-derived, anti-cancer agent kahalalide F

2001 ◽  
Vol 12 (7) ◽  
pp. 575-582 ◽  
Author(s):  
Rolf W Sparidans ◽  
Ellen Stokvis ◽  
José M Jimeno ◽  
Luis López-Lázaro ◽  
Jan HM Schellens ◽  
...  
Keyword(s):  
The Novel ◽  
Enzymatic Stability ◽  
Cyclic Depsipeptide ◽  
Kahalalide F ◽  
Anti Cancer ◽  
Cancer Agent

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.

Abstract 931: From bench to bedside: Using ProTide chemistry to transform 3'-deoxyadenosine into the novel anti-cancer agent Nuc-7738

2021 ◽  
Author(s):  
Hagen Schwenzer ◽  
Michaela Serpi ◽  
Valentina Ferrari ◽  
James Chettle ◽  
Josephine Morris ◽  
...  
Keyword(s):  
The Novel ◽  
Anti Cancer ◽  
Cancer Agent

scholarly journals Coconut: Natural Source of Potential Anti Cancer Agent

CORD ◽  
2016 ◽  
Vol 32 (1) ◽  
pp. 9
Author(s):  
Dr. Amit Ghosh
Keyword(s):  
Drug Development ◽  
Cocos Nucifera ◽  
Drug Repurposing ◽  
Natural Source ◽  
The Novel ◽  
Treatment Development ◽  
Current Strategy ◽  
Anticancer Effects ◽  
Anti Cancer ◽  
Cancer Agent

The current strategy of drug development is time consuming and expensive. This contrasts sharply with the vision of affordable drug development. The costly and the lengthy paradigm of drug discoveries are major obstacles for combating with rapidly emerging and sporadic diseases. The dichotomy between the urgent requirement of affordable treatment development and the hindrance it faces is apparent in several recent literatures which reflects the importance of drug repurposing and development of botanical drugs. Consistent with this idea, past few decades of studies on Cocos nucifera has yielded a fair knowledge about the anticancer potential of coconut products. The aggregate knowledge is undeniably positive and offers the novel avenues for the therapeutics and affordable drug development. This article highlights the link between coconut products and its anticancer effects.

scholarly journals Dimethyl Fumarate Induces Metabolic Crisie to Suppress Pancreatic Carcinoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Kaiyuan Chen ◽  
Shanshan Wu ◽  
Sisi Ye ◽  
Huimin Huang ◽  
Yi Zhou ◽  
...  
Keyword(s):  
Cell Death ◽  
Aerobic Glycolysis ◽  
Dimethyl Fumarate ◽  
Pharmacological Activities ◽  
Novel Therapy ◽  
Docking Analysis ◽  
Downstream Target ◽  
Anti Cancer ◽  
Psoriasis Therapy ◽  
Cancer Agent

Dimethyl fumarate (DMF) is an approved drug used in the treatment of multiple sclerosis (MS) and psoriasis therapy. Multiple studies have demonstrated other pharmacological activities of DMF such as an anti-cancer agent. In particular, studies have shown that DMF can modulate the NRF2/HO1/NQO1 antioxidant signal pathway and inactivate NF-κB to suppress the growth of colon and breast cancer cells, and induce cell death. In this study, we aimed to evaluate the anti-tumor activities of DMF in pancreatic cancer (PC) focusing on cell death as the predominant mechanism of response. We showed that both mitochondrial respiration and aerobic glycolysis were severely depressed following treatment with DMF and the effects could be abrogated by treatment with L-cysteine and N-acetyl-L-cysteine (NAC). Importantly, we verified that DMF induced metabolic crisis and that cell death was not related to alterations in ROS. Our data implied that MTHFD1 could be a potential downstream target of DMF identified by molecular docking analysis. Finally, we confirmed that MTHFD1 is up-regulated in PC and overexpression of MTHFD1 was negatively related to outcomes of PC patients. Our data indicate that DMF induces metabolic crisie to suppress cell growth and could be a potential novel therapy in the treatment of PC.

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