Herbal formula YYJD inhibits tumor growth by inducing cell cycle arrest and senescence in lung cancer

Zheng, Tingting; Que, Zujun; Jiao, Lijing; Kang, Yani; Gong, Yabin; Yao, Jialin; Ma, Chi; Bi, Ling; Dong, Qihan; Zhao, Xiaodong; Xu, Ling

doi:10.1038/s41598-017-05146-x

Cited by 19 publications

(23 citation statements)

References 35 publications

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“…Cell cycle progression plays an important role in tumour growth, and its regulation is an effective strategy to control tumour growth. It has been reported that the active ingredients of traditional Chinese medicine can arrest tumour cells at different cell cycle, which in turn inhibit tumour cell growth, proliferation, and induce apoptosis [16] [17]. In present study, Acetylshikonin blocked cell cycle progression at G0/G1 phase, which demonstrated that Acetylshikonin interfered with the normal tumour cell cycle and inhibited tumour growth.…”

Section: Acetylshikonin Inhibited the Growth Of Xenografted Tumours Isupporting

confidence: 57%

Acetylshikonin Inhibits Colorectal Cancer Growth via PI3K/Akt/mTOR Signaling Pathway

Zhu¹,

Zhong²,

Zhou³

et al. 2018

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Background: Acetylshikonin, a major constituent isolated from Arnebia euchroma, is a potential candidate for anti-colorectal cancer drugs. However, the potential activity and underlying mechanism of Acetylshikonin against colorectal cancer remain unclear. Methods: In this study, Acetylshikonin was isolated from the active CHCl3 extract of Arnebia euchroma using activity-guided screening, and elucidated by the extensive spectroscopic analysis and comparison with literature data. Human colorectal cancer cells HT29, DLD-1, HCT116 or Caco-2 were exposed to different concentrations of Acetylshikonin (6.25 -100 μg/mL) for 24 or 48 h. Cell viability, cell apoptosis and cell cycle distribution were detected. The activity of Acetylshikonin and potential mechanism of the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway were evaluated in vitro and vivo. Results: We found that Acetylshikonin exhibited remarkable anti-proliferative activity in a dose-dependent manner against HT29 cells with the IC50 values of 60.82 μg/ml and 30.78 μg/ml at 24, 48 h, respectively. Moreover, Acetylshikonin induced cell cycle arrest at G0/G1 phase and early apoptosis through inhibition of PI3K/Akt/mTOR pathway. Furthermore, the assays of cell inhibition, early

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Section: Acetylshikonin Inhibited the Growth Of Xenografted Tumours Isupporting

confidence: 57%

Acetylshikonin Inhibits Colorectal Cancer Growth via PI3K/Akt/mTOR Signaling Pathway

Zhu¹,

Zhong²,

Zhou³

et al. 2018

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“…Our previous studies indicated that it induces cellular apoptosis through activation of FAS and DR4, and exerts synergistic effects in combination with chemotherapy on lung cancer cell apoptosis . Using computational algorithms, recently we optimized the ingredients of JFK formula and the optimized formula Yangyinjiedu (YYJD) exhibits anti‐tumour effect by inducing lung cancer cell senescence . In this study, we further examined the anti‐tumour mechanism of YYJD and demonstrated that YYJD induces apoptosis by activating transcriptional regulator EGR1 in lung cancer cells.…”

Section: Introductionmentioning

confidence: 94%

Herbal formula Yangyinjiedu induces lung cancer cell apoptosis via activation of early growth response 1

Yang

Kang

Zhao

et al. 2019

J Cellular Molecular Medi

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Traditional Chinese Medicine (TCM) has been extensively used in clinical practices and proven to be effective against cancer. However, the underlying mechanisms remain to be investigated. In this study, we examined the anticancer activities of Chinese herbal formula Yangyinjiedu (YYJD) and found that YYJD exhibits cytotoxicity against lung cancer cells. Transcriptome analysis indicated that 2178 genes were differentially expressed (P < 0.05) upon YYJD treatment, with 1464 being (67.2%) up‐regulated. Among these, we found that the tumour suppressor early growth response 1 (EGR1) is the most activated. We demonstrated that EGR1 contributes to YYJD‐induced apoptosis in A549. Through dissecting EGR1‐associated transcriptional network, we identified 275 genes as EGR1 direct targets, some targets are involved in apoptosis. Lastly, we observed that YYJD enhances EGR1 expression and induces cell death in tumour xenografts. Collectively, these findings suggest that YYJD exerts its anticancer activities through EGR1 activation, thus providing the evidence for its potential clinical application for lung cancer patients.

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“…For in vitro experiments, a quantified amount (50 mL) of the GJXLT extract was processed with a freeze dryer to obtain crystal powder. Freeze-dried powder was dissolved in culture medium and filtered and stored as a stock solution (142 mg/mL) at -20°C [ 11 ].…”

Section: Methodsmentioning

confidence: 99%

In Vitro and In Vivo Inhibitory Effect of Gujin Xiaoliu Tang in Non‐Small Cell Lung Cancer

Hou

Zhou

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Non-small cell lung cancer (NSCLC) is a serious threat to people's health. This study aims to determine the possible effect of Gujin Xiaoliu Tang (GJXLT) on NSCLC, which is an empirical formula from Professor Dai-Han Zhou. In this study, chromatographic fingerprinting of GJXLT and A549 cell model in vitro and in vivo was established. We cultured A549 cells in vitro and found that GJXLT inhibited A549 cell growth and induced apoptosis. Compared with the control group, the expression of p-STAT3 and VEGF proteins in the GJXLT groups was decreased. Similar findings were also observed in vivo. First, GJXLT inhibited the growth of transplanted tumor and did not reduce the weight of the tumor-bearing mice in comparison with that of the control group. Then, the Ki-67 expression of transplanted tumor in the GJXLT groups was decreased. In addition, the apoptosis rate of transplanted tumor in the GJXLT groups was increased. Overall, our data showed that GJXLT inhibited A549 cell proliferation and induced apoptosis in vivo and in vitro. Furthermore, GJXLT inhibited the growth of lung cancer xenograft in nude mice model with no obvious side effects. The anti-tumor effect of GJXLT might also be related to the inhibition of p-STATS and VEGF expression in the JAK2/STAT3 pathway. Our results demonstrated the potential of GJXLT as a novel treatment for NSCLC.

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Herbal formula YYJD inhibits tumor growth by inducing cell cycle arrest and senescence in lung cancer

Cited by 19 publications

References 35 publications

Acetylshikonin Inhibits Colorectal Cancer Growth via PI3K/Akt/mTOR Signaling Pathway

Acetylshikonin Inhibits Colorectal Cancer Growth via PI3K/Akt/mTOR Signaling Pathway

Herbal formula Yangyinjiedu induces lung cancer cell apoptosis via activation of early growth response 1

In Vitro and In Vivo Inhibitory Effect of Gujin Xiaoliu Tang in Non‐Small Cell Lung Cancer

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