Acetylcholinesterase expression mediated by c-Jun-NH2-terminal kinase pathway during anticancer drug-induced apoptosis

Deng, Rong; Li, W.; Guan, Zhi‐Zhong; Zhou, Jingming; Wang, Y.; Yu, Mei; Li, M. T.; Feng, Gong Kan; Huang, Wenlin; Liu, Z. C.; Han, Yifan; Zeng, Yi‐Xin; Zhu, Xiao Feng

doi:10.1038/sj.onc.1209686

Cited by 60 publications

(52 citation statements)

References 33 publications

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“…For example, ExcisaninA extracted from Rabdosia excisa and its semisynthetic analogues shows significant cytotoxic activity against P388 murine leukemia cells (33,34). We have also shown that ExcisaninA isolated from Isodon MacrocalyxinD could inhibit human colon cancer SW620 cells proliferation (35). In the present study, ExcisaninA not only showed its significantly inhibitory effect on Hep3B and MDA-MB-453 cells proliferation alone but also produced synergistic growth inhibition effect with other anticancer drugs in vitro (Fig.…”

Section: Discussionsupporting

confidence: 48%

ExcisaninA, a diterpenoid compound purified from Isodon MacrocalyxinD, induces tumor cells apoptosis and suppresses tumor growth through inhibition of PKB/AKT kinase activity and blockade of its signal pathway

Deng

Tang

Xia

et al. 2009

Molecular Cancer Therapeutics

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Section: Discussionsupporting

confidence: 48%

ExcisaninA, a diterpenoid compound purified from Isodon MacrocalyxinD, induces tumor cells apoptosis and suppresses tumor growth through inhibition of PKB/AKT kinase activity and blockade of its signal pathway

Deng

Tang

Xia

et al. 2009

Molecular Cancer Therapeutics

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“…Reverse transcription-PCR was performed as previously described (Deng et al, 2006). These primers for Mre11 (sense: 5 0 -TCAACTTTGGGAAACTTAT C-3 0 , antisense: 5 0 -GAAGGCTGCTGTCTTGTAG-3 0 ) were designed to generate a fragment of 577 bp.…”

Section: Western Blot Analysismentioning

confidence: 99%

PKB/Akt promotes DSB repair in cancer cells through upregulating Mre11 expression following ionizing radiation

Deng

Tang

et al. 2010

Oncogene

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“…Cells were treated with the indicated conditions, and then the total RNA was isolated by TRIzol (Invitrogen) according to the manufacturer's instructions. The reverse transcription polymerase chain reaction reactions were done as previously described (38).…”

Section: Primers and Reverse Transcription Polymerase Chain Reactionmentioning

confidence: 99%

G-quadruplex ligand SYUIQ-5 induces autophagy by telomere damage and TRF2 delocalization in cancer cells

Zhou

Deng

Zhang

et al. 2009

Molecular Cancer Therapeutics

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Agents stabilizing G-quadruplexes have the potential to destroy the functional structure of telomere and could therefore act as antitumor agents. We previously reported that SYUIQ-5 could stabilize G-quadruplex, induce senescence, and inhibit c-myc gene promoter activity. In this study, we showed that SYUIQ-5 inhibited proliferation of CNE2 and HeLa cancer cells, triggered a rapid and potent telomere DNA damage response characterized by the formation of telomeric foci γ-H2AX, and obviously induced autophagy with the features of increased LC3-II and a punctuated pattern of YFP-LC3 fluorescence. These phenomena may primarily depend on the delocalization of TRF2 from telomere, which was further degraded by proteasomes. Furthermore, overexpression of TRF2 inhibited SYUIQ-5-induced γ-H2AX expression. Also, ATM was activated following SYUIQ-5 treatment. The pretreatment with ATM inhibitor ku55933 and ATM siRNA effectively reduced the production of γ-H2AX and LC3-II. ATM knockdown partially antagonized the anticancer effects of SYUIQ-5. Moreover, inhibition of autophagy by short hairpin RNA against the autophagy-related gene ATG5 attenuated the cytotoxicity of SYUIQ-5. These results indicated that SYUIQ-5 triggered potent telomere damage through TRF2 delocalization from telomeres, and eventually induced autophagic cell death in cancer cells. Our findings exhibit a novel mechanism that is responsible for the antitumor effects of SYUIQ-5. [Mol Cancer Ther 2009;8 (12):3203-13]

show abstract

Acetylcholinesterase expression mediated by c-Jun-NH2-terminal kinase pathway during anticancer drug-induced apoptosis

Cited by 60 publications

References 33 publications

ExcisaninA, a diterpenoid compound purified from Isodon MacrocalyxinD, induces tumor cells apoptosis and suppresses tumor growth through inhibition of PKB/AKT kinase activity and blockade of its signal pathway

ExcisaninA, a diterpenoid compound purified from Isodon MacrocalyxinD, induces tumor cells apoptosis and suppresses tumor growth through inhibition of PKB/AKT kinase activity and blockade of its signal pathway

PKB/Akt promotes DSB repair in cancer cells through upregulating Mre11 expression following ionizing radiation

G-quadruplex ligand SYUIQ-5 induces autophagy by telomere damage and TRF2 delocalization in cancer cells

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