Repression of phosphoinositide-dependent protein kinase 1 expression by ciglitazone via Egr-1 represents a new approach for inhibition of lung cancer cell growth

Hann, Swei Sunny; Tang, Qing; Zheng, Fang; Zhao, Shunyu; Chen, Jianping; Wang, Zhiyu

doi:10.1186/1476-4598-13-149

Cited by 24 publications

(16 citation statements)

References 43 publications

(56 reference statements)

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“…It can be induced by a wide range of extracellular stimuli (including growth factors and cytokines) and activates the downstream target genes through the consensus GC‐rich sequence 5’‐ MCGCCCACDC‐3’0 . Recently, it has been reported that the compound ciglitazone induces EGR‐1 and leads to inhibition of lung cancer cell proliferation . In this study, we observed that TCM YYJD induces proliferation inhibition and apoptosis in lung cancer cells (Figure A).…”

Section: Discussionmentioning

confidence: 50%

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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Section: Discussionmentioning

confidence: 50%

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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“…AMPK plays a central role in the control of cell growth, apoptosis, and autophagy through the regulation of several downstream effectors in cancer cells [ 30 ]. The activation of AMPK signaling in mediating the physiopathological responses of cancer cell survival has been shown in other studies [ 31 , 32 ]. Reports from our study and other studies indicated that activation of AMPK contributed to the increase in IGFBP1 and FOXO3a proteins expression, the decrease in cancer cell growth, and other functions in several cell systems including lung cancer [ 33 – 36 ].…”

Section: Discussionmentioning

confidence: 60%

Chinese Herbal Medicine Fuzheng Kang‐Ai Decoction Inhibited Lung Cancer Cell Growth through AMPKα‐Mediated Induction and Interplay of IGFBP1 and FOXO3a

Zheng¹,

Wu²,

Li³

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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The aim of this study is to investigate the actions of Chinese herbal medicine, called “Fuzheng Kang-Ai” (FZKA for short) decoction, against non-small cell lung cancer (NSCLC) and its mechanisms in vitro and in vivo. We showed that the effect of FZKA decoction significantly inhibited growth of A549 and PC9 cells. Furthermore, FZKA increased phosphorylation of AMP-activated protein kinase alpha (AMPKα) and induced protein expression of insulin-like growth factor (IGF) binding protein 1 (IGFBP1) and forkhead homeobox type O3a (FOXO3a). The specific inhibitor of AMPKα (Compound C) blocked FZKA-induced protein expression of IGFBP1 and FOXO3a. Interestingly, silencing of IGFBP1 and FOXO3a overcame the inhibitory effect of FZKA on cell growth. Moreover, silencing of IGFBP1 attenuated the effect of FZKA decoction on FOXO3a expression, and exogenous expression of FOXO3a enhanced the FZKA-stimulated phosphorylation of AMPKα. Accordingly, FZKA inhibited the tumor growth in xenograft nude mice model. Collectively, our results show that FZKA decoction inhibits proliferation of NSCLC cells through activation of AMPKα, followed by induction of IGFBP1 and FOXO3a proteins. Exogenous expression of FOXO3a feedback enhances FZKA decoction-stimulated IGFBP1 expression and phosphorylation of AMPKα. The reciprocal interplay of IGFBP1 and FOXO3a contribute to the overall responses of FAKA decoction.

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“…The Caspase 3 Activity Assay Kit (Beyotime Institute of Biotechnology, Jiangsu, China) was used to evaluate the effect of DOX/DQA-DOX@DSPE-hyd-PEG-AA on the activity of caspase3 in tumor cell 37 . Briefly, cells were seeded in dishes and incubated for 24 h. The culture medium was replaced by fresh culture medium that contained different concentration of DOX, DQA-DOX, DOX@DSPE-hyd-PEG-AA and DOX/DQA-DOX@DSPE-hyd-PEG-AA.…”

Section: Methodsmentioning

confidence: 99%

Dual subcellular compartment delivery of doxorubicin to overcome drug resistant and enhance antitumor activity

Song

Liu

Cheng

et al. 2015

Sci Rep

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In order to overcome drug resistant and enhance antitumor activity of DOX, a new pH-sensitive micelle (DOX/DQA-DOX@DSPE-hyd-PEG-AA) was prepared to simultaneously deliver DOX to nucleus and mitochondria. Drug released from DOX/DQA-DOX@DSPE-hyd-PEG-AA showed a pH-dependent manner. DOX/DQA-DOX@DSPE-hyd-PEG-AA induced the depolarization of mitochondria and apoptosis in MDA-MB-231/ADR cells and A549 cells, which resulted in the high cytotoxicity of DOX/DQA-DOX@DSPE-hyd-PEG-AA against MDA-MB-231/ADR cells and A549 cells. Confocal microscopy confirmed that DOX/DQA-DOX@DSPE-hyd-PEG-AA simultaneously delivered DQA-DOX and DOX to the mitochondria and nucleus of tumor cell. After DOX/DQA-DOX@DSPE-hyd-PEG-AA was injected to the tumor-bearing nude mice by the tail vein, DOX was mainly found in tumor tissue. But DOX was widely distributed in the whole body after the administration of free DOX. Compared with free DOX, the same dose of DOX/DQA-DOX@DSPE-hyd-PEG-AA significantly inhibited the growth of DOX-resistant tumor in tumor-bearing mice without obvious systemic toxicity. Therefore, dual subcellular compartment delivery of DOX greatly enhanced the antitumor activity of DOX on DOX-resistant tumor. DOX/DQA-DOX@DSPE-hyd-PEG-AA has the potential in target therapy for DOX-resistant tumor.

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Repression of phosphoinositide-dependent protein kinase 1 expression by ciglitazone via Egr-1 represents a new approach for inhibition of lung cancer cell growth

Cited by 24 publications

References 43 publications

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

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

Chinese Herbal Medicine Fuzheng Kang‐Ai Decoction Inhibited Lung Cancer Cell Growth through AMPKα‐Mediated Induction and Interplay of IGFBP1 and FOXO3a

Dual subcellular compartment delivery of doxorubicin to overcome drug resistant and enhance antitumor activity

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