Beneficial Outcomes of Kimchi Prepared with Amtak Baechu Cabbage and Salting in Brine Solution: Anticancer Effects in Pancreatic and Hepatic Cancer Cells

2018 ◽  
Vol 37 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Gyl-Hoon Song ◽  
Eui-Seong Park ◽  
Seung-Min Lee ◽  
Dong-Bok Park ◽  
Kun-Young Park
Keyword(s):  
Cancer Cells ◽  
Hepatic Cancer ◽  
Brine Solution ◽  
Anticancer Effects

Construction of recombinant adenovirus vectors containing Akt gene and its effect on survival of hepatic cancer cells

2012 ◽  
Vol 32 (3) ◽  
pp. 332-335
Author(s):  
Ke-he CHEN ◽  
Ze-long HAN ◽  
Jian-jun LI ◽  
Jin-fei PAN ◽  
An-ling LIU
Keyword(s):  
Cancer Cells ◽  
Recombinant Adenovirus ◽  
Hepatic Cancer ◽  
Adenovirus Vectors

Vitamin C as an Anticancer Agent: Regulation of Signaling Pathways

2020 ◽  
Vol 20 (21) ◽  
pp. 1868-1875
Author(s):  
Ghazala Butt ◽  
Ammad A. Farooqi ◽  
Aima Adylova ◽  
Rukset Attar ◽  
Seher Yilmaz ◽  
...  
Keyword(s):  
Vitamin C ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Scientific Evidence ◽  
Treatment Options ◽  
Published Data ◽  
New Era ◽  
Molecular Oncology ◽  
Anticancer Effects ◽  
Oncogenic Pathways

Treatment options for effective treatment of cancer with minimum off-target effects and maximum clinical outcomes have remained overarching goals in the clinical oncology. Vitamin C has remained in the shadows of controversy since the past few decades; burgeoning evidence has started to shed light on wide-ranging anticancer effects exerted by Vitamin C to induce apoptosis in drug-resistant cancer cells, inhibit uncontrolled proliferation of the cancer cells and metastatic spread. Landmark achievements in molecular oncology have ushered in a new era, and researchers have focused on the identification of oncogenic pathways regulated by Vitamin C in different cancers. However, there are visible knowledge gaps in our understanding related to the ability of Vitamin C to modulate a myriad of transduction cascades. There are scattered pieces of scientific evidence about promising potential of Vitamin C to regulate JAK-STAT, TGF/SMAD, TRAIL and microRNAs in different cancers. However, published data is insufficient and needs to be investigated comprehensively to enable basic and clinical researchers to reap full benefits and promote result-oriented transition of Vitamin C into various phases of clinical trials. In this review, we will emphasize on available evidence related to the regulation of oncogenic cell signaling pathways by Vitamin C in different cancers. We will also highlight the conceptual gaps, which need detailed and cutting-edge research.

scholarly journals α-Pinene Enhances the Anticancer Activity of Natural Killer Cells via ERK/AKT Pathway

2021 ◽  
Vol 22 (2) ◽  
pp. 656
Author(s):  
Hantae Jo ◽  
Byungsun Cha ◽  
Haneul Kim ◽  
Sofia Brito ◽  
Byeong Mun Kwak ◽  
...  
Keyword(s):  
Nk Cells ◽  
Cancer Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Granzyme B ◽  
Akt Pathway ◽  
Cell Cytotoxicity ◽  
Anticancer Effects ◽  
Nk Cell Cytotoxicity

Natural killer (NK) cells are lymphocytes that can directly destroy cancer cells. When NK cells are activated, CD56 and CD107a markers are able to recognize cancer cells and release perforin and granzyme B proteins that induce apoptosis in the targeted cells. In this study, we focused on the role of phytoncides in activating NK cells and promoting anticancer effects. We tested the effects of several phytoncide compounds on NK-92mi cells and demonstrated that α-pinene treatment exhibited higher anticancer effects, as observed by the increased levels of perforin, granzyme B, CD56 and CD107a. Furthermore, α-pinene treatment in NK-92mi cells increased NK cell cytotoxicity in two different cell lines, and immunoblot assays revealed that the ERK/AKT pathway is involved in NK cell cytotoxicity in response to phytoncides. Furthermore, CT-26 colon cancer cells were allografted subcutaneously into BALB/c mice, and α-pinene treatment then inhibited allografted tumor growth. Our findings demonstrate that α-pinene activates NK cells and increases NK cell cytotoxicity, suggesting it is a potential compound for cancer immunotherapy.

scholarly journals Anticancer effects of bifidobacteria on colon cancer cell lines

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zeinab Faghfoori ◽  
Mohammad Hasan Faghfoori ◽  
Amir Saber ◽  
Azimeh Izadi ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Rt Pcr ◽  
Anticancer Effects ◽  
Colon Cancer Cell Lines ◽  
Apoptotic Genes

Abstract Background Colorectal cancer (CRC), with a growing incidence trend worldwide, is resistant to apoptosis and has uncontrolled proliferation. It is recently reported that probiotic microorganisms exert anticancer effects. The genus Bifidobacterium, one of the dominant bacterial populations in the gastrointestinal tract, has received increasing attention because of widespread interest in using it as health-promoting microorganisms. Therefore, the present study aimed to assess the apoptotic effects of some bifidobacteria species on colon cancer cell lines. Methods The cytotoxicity evaluations performed using MTT assay and FACS-flow cytometry tests. Also, the effects of five species of bifidobacteria secretion metabolites on the expression level of anti- or pro-apoptotic genes including BAD, Bcl-2, Caspase-3, Caspase-8, Caspase-9, and Fas-R studied by real-time polymerase chain reaction (RT-PCR) method. Results The cell-free supernatant of all studied bifidobacteria significantly decreased the survival rates of colon cancer cells compared with control groups. Flow cytometric and RT-PCR results indicated that apoptosis is induced by bifidobacteria secretion metabolites and the mechanism for the action of bifidobacteria species in CRC prevention could be down-regulation and up-regulation of anti-apoptotic and, pro-apoptotic genes. Conclusions In the present study, different bifidobacteria species showed anticancer activity on colorectal cancer cells through down-regulation and up-regulation of anti-apoptotic and pro-apoptotic genes. However, further studies are required to clarify the exact mechanism of apoptosis induction by bifidobacteria species.

scholarly journals Pharmacological Levels of Withaferin A (Withania somnifera) Trigger Clinically Relevant Anticancer Effects Specific to Triple Negative Breast Cancer Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e87850 ◽  
Author(s):  
Katarzyna Szarc vel Szic ◽  
Ken Op de Beeck ◽  
Dariusz Ratman ◽  
An Wouters ◽  
Ilse M. Beck ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Withania Somnifera ◽  
Triple Negative ◽  
Withaferin A ◽  
Anticancer Effects

scholarly journals Synthesis of Novel FTY720 Analogs with Anticancer Activity through PP2A Activation

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2750 ◽  
Author(s):  
Jitendra Shrestha ◽  
Sung Ki ◽  
Sang Shin ◽  
Seon Kim ◽  
Joo-Youn Lee ◽  
...  
Keyword(s):  
Cell Viability ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Sphingosine Kinase ◽  
Basic Structure ◽  
Docking Study ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
Anticancer Effects ◽  
Pp2a Activation

FTY720 inhibits various cancers through PP2A activation. The structure of FTY720 is also used as a basic structure for the design of sphingosine kinase (SK) inhibitors. We have synthesized derivatives using an amide chain in FTY720 with a phenyl backbone, and then compounds were screened by an MTT cell viability assay. The PP2A activity of compound 7 was examined. The phosphorylation levels of AKT and ERK, downstream targets of PP2A, in the presence of compound 7, were determined. Compound 7 may exhibit anticancer effects through PP2A activation rather than the mechanism by inhibition of SK1 in cancer cells. In the docking study of compound 7 and PP2A, the amide chain of compound 7 showed an interaction with Asn61 that was different from FTY720, which is expected to affect the activity of the compound.

Daidzein causes cytochrome c-mediated apoptosis via the Bcl-2 family in human hepatic cancer cells

2013 ◽  
Vol 60 ◽  
pp. 542-549 ◽  
Author(s):  
Hyun Jin Park ◽  
Young Keul Jeon ◽  
Dong Hun You ◽  
Myeong Jin Nam
Keyword(s):  
Cytochrome C ◽  
Cancer Cells ◽  
Hepatic Cancer

scholarly journals Dual effects of the Nrf2 inhibitor for inhibition of hepatitis C virus and hepatic cancer cells

BMC Cancer ◽  
2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Yuko Murakami ◽  
Kazuo Sugiyama ◽  
Hirotoshi Ebinuma ◽  
Nobuhiro Nakamoto ◽  
Keisuke Ojiro ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cancer Cells ◽  
Hepatic Cancer

scholarly journals Emetine Synergizes with Cisplatin to Enhance Anti-Cancer Efficacy against Lung Cancer Cells

2019 ◽  
Vol 20 (23) ◽  
pp. 5914 ◽  
Author(s):  
Ti-Hui Wu ◽  
Shan-Yueh Chang ◽  
Yu-Lueng Shih ◽  
Tsai-Wang Huang ◽  
Hung Chang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Clinical Problem ◽  
Driver Mutations ◽  
Anticancer Efficacy ◽  
Lung Cancers ◽  
Anticancer Effects ◽  
Therapeutic Choice ◽  
Reporter Assays

Cisplatin is still the primary therapeutic choice for advanced lung cancers without driver mutations. The occurrence of cisplatin resistance is a major clinical problem in lung cancer treatment. The natural extracted agent emetine reportedly has anticancer effects. This study aimed to explore the possible role of emetine in cisplatin resistance. We used cell viability, Western blot, and Wnt reporter assays to show that emetine suppresses proliferation, β-catenin expression, and Wnt/β-catenin signaling in non-small cell lung cancer (NSCLC). The synergism of emetine and cisplatin was assessed by constructing isobolograms and calculating combination index (CI) values using the Chou-Talalay method. Emetine effectively synergized with cisplatin to suppress the proliferation of cancer cells. Furthermore, nuclear β-catenin and cancer stem cell-related markers were upregulated in the cisplatin-resistant subpopulation of CL1-0 cells. Emetine enhanced the anticancer efficacy of cisplatin and synergized with cisplatin in the cisplatin-resistant subpopulation of CL1-0 cells. Taken together, these data suggest that emetine could suppress the growth of NSCLC cells through the Wnt/β-catenin pathway and contribute to a synergistic effect in combination with cisplatin.

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