Traditional Chinese Medicine <scp>CFF</scp>‐1 induced cell growth inhibition, autophagy, and apoptosis via inhibiting <scp>EGFR</scp>‐related pathways in prostate cancer

Wu, Zhaomeng; Zhu, Qingyi; Yin, Yingying; Kang, Dan; Cao, Runyi; Tian, Qian; Lu, Shan; Liu, Ping

doi:10.1002/cam4.1419

Cited by 26 publications

(20 citation statements)

References 42 publications

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“…A previous study demonstrated that the PI3K/Akt signaling pathway is inactivated, whereas osthole promotes the apoptosis of esophageal squamous cell carcinoma ( 48 ). Furthermore, repression of the PI3K/Akt signaling pathway inhibits cell viability and may enhance the apoptosis of PCa ( 49 ), indicating the role of the PI3K/Akt signaling pathway during tumor progression. Thus, the expression of PI3K and Akt was determined in the present study in order to explore the role of the PI3K/Akt pathway in the antitumor effect of si-ASF1B.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

et al. 2018

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Prostate cancer (PCa) is one of the most common malignancies among males worldwide. Anti-silencing function 1B histone chaperone (ASF1B) has been reported to be involved in PCa. The present study aimed to investigate the role and molecular mechanism of ASF1B in PCa. Data of genes were obtained from The Cancer Genome Atlas data- base. The core gene was identified using the DAVID website. Cell viability and colony formation were detected using a cell counting kit-8 assay and crystal violet staining, respectively. Cell cycle distribution and apoptosis were assessed using flow cytometry analysis. The corresponding factors were analyzed by reverse transcription-quantitative polymerase chain reaction and western blotting. It was demonstrated that ASF1B was highly expressed in the PCa tissues and cells compared with the non-PCa tissues and cells, respectively. While siRNA-ASF1B significantly reduced the viability and colony formation, it promoted apoptosis, G1 phase cell cycle arrest of LNCap as well as C4-2 cells. siRNA-ASF1B was revealed to significantly reduce the level of B-cell lymphoma-2 and cyclin D1, and enhance the expression levels of p53, caspase-3 and Bcl-2 associated X protein. Furthermore, the phosphorylation levels of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (Akt) were significantly decreased in the siRNA-ASF1B group compared with the mock group. In summary, the present study demonstrated that silencing of ASF1B suppressed the proliferation, and promoted apoptosis and cell cycle arrest of PCa cells. Inhibition of the PI3K/Akt signaling pathway was pertinent to the role of si-ASF1B. This phenomenon suggests that the downregulation of ASF1B may aid in inhibiting the progression of PCa.

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Section: Discussionmentioning

confidence: 99%

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

et al. 2018

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“…It is well known that antitumor drugs and related genes generally inhibit the growth of cancer cells and promote apoptosis. Proliferation and apoptosis are 2 important processes of tumor development [ 29 – 32 ]. Yang et al have confirmed that MTHFD1L silencing can repress viability of esophageal squamous cancer cells and expedite apoptosis [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Methylenetetrahydrofolate Dehydrogenase 1 Silencing Expedites the Apoptosis of Non-Small Cell Lung Cancer Cells via Modulating DNA Methylation

Jiang

Chen

et al. 2018

Med Sci Monit

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BackgroundNon-small cell lung cancer (NSCLC) accounts for about 85% of all types of lung cancer. Methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) is involved in DNA methylation, and DNA methylation is related to tumorigenesis. The role of MTHFD1 in NSCLC was examined in our study.Material/MethodsThe correlation between the expression of MTHFD1 and the clinicopathological features of patients diagnosed with lung cancer was investigated using the chi-square test. The viability and apoptosis of NCI-H1299 cells was respectively detected using cell counting kit-8 and flow cytometry assays. The expression levels of MTHFD1, apoptosis-related factors and DNA methyltransferase-related factors were assessed by quantitative real-time PCR (qRT-PCR) and western blot assays.ResultsWe found that MTHFD1 expression in the tumor tissues and cells was higher than that of adjacent normal tissues and cells. The survival time of patients with high MTHFD1 expression was shorter than those with low MTHFD1 expression. The expression level of MTHFD1 was related to tumor size, TNM stage, histologic grade, and metastasis, but not linked to gender and age. Besides, si-MTHFD1 significantly decreased the viability of cells in a time-dependent manner, and increased cell apoptosis. When cells were transfected with MTHFD1-siRNA, the levels of surviving and B-cell lymphoma-2 (Bcl-2) were attenuated, while p53 and Bcl-2 associated X protein (Bax) levels were enhanced. Moreover, si-MTHFD1 markedly downregulated the expression levels of DNA methyltransferase 1 (DNMT1), DNMT3a, and DNMT3b.ConclusionsCollectively, our results proved that MTHFD1 silencing obviously reduced the proliferation and enhanced the apoptosis of NSCLC via suppressing DNA methylation.

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“…Although immunotherapy and targeted therapy are used in many tumors, these treatments are rarely used in VSCC patients at present. Some traditional Chinese medicines have been confirmed to be effective anti‐tumor agents (Song, Yang, Bai, & Ji, ; Wang, Zhao, Wu, Guan, & Wu, ; Wu et al, ). However, there have been no reports regarding the research on AS‐IV in VSCC.…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV inhibits cell proliferation in vulvar squamous cell carcinoma through the TGF‐β/Smad signaling pathway

Zhao

Wang

et al. 2018

Dermatologic Therapy

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Objective To explore the inhibition of the proliferation of vulvar squamous cell carcinoma (VSCC) by astragaloside IV. Methods MTT examined the cell proliferation of VSCC. Flow cytometry analyzed cell cycle and apoptosis. Western blot assay detected the expression of some relevant proteins. Results AS‐IV reduced the proliferation of SW962 cells in a concentration‐ and time‐dependent manner, induced cell‐cycle arresting in G0/G1 phase, as demonstrated by the up‐regulation of P53 and P21 expression, and the down‐regulation of cyclin D1 expression. AS‐IV enhanced the expression of Bax and cleaved‐caspase 3, and suppressed Bcl‐2 and Bcl‐xl expression, which resulted in apoptosis increased. Furthermore, the expression of Beclin‐1 and LC3‐B was upregulated and that of P62 was downregulated, which suggested that AS‐IV could increase the incidence of autophagy in SW962 cells. After inhibiting autophagy by 3‐methyladenine (3‐MA), cell apoptosis decreased upon AS‐IV treatment. Similarly, TGF‐β1 stimulated SW962 cells, cell proliferation enhanced, and the expression of TGF‐βRII and Smad4 was decreased. Furthermore, the expression of proteins that promote apoptosis and autophagy decreased. After AS‐IV treatment, the expression levels of the above proteins exhibited the opposite effect. Conclusion AS‐IV inhibits cell proliferation and induces apoptosis and autophagy through the TGF‐β/Smad signaling pathway in VSCC.

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Traditional Chinese Medicine CFF‐1 induced cell growth inhibition, autophagy, and apoptosis via inhibiting EGFR‐related pathways in prostate cancer

Cited by 26 publications

References 42 publications

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

Methylenetetrahydrofolate Dehydrogenase 1 Silencing Expedites the Apoptosis of Non-Small Cell Lung Cancer Cells via Modulating DNA Methylation

Astragaloside IV inhibits cell proliferation in vulvar squamous cell carcinoma through the TGF‐β/Smad signaling pathway

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