Suppression of hepatocarcinoma model in vitro and in vivo by ECRG2 delivery using adenoviral vector

Song, Haiqu; Song, Chongwen; Wang, H; C, Li; Yang, Fang; Lu, Shan; Lin, Chen; Zhan, Qimin; Wang, X; Qian, Haili

doi:10.1038/cgt.2012.77

Cited by 11 publications

(16 citation statements)

References 14 publications

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“…1,2 Studies have also determined that overexpressed ECRG2 induced cell death in cultured cancer cells 5 and adenovirally expressed ECRG2 inhibited grafted tumors grown in nude mice. 6 ECRG2 has been demonstrated to inhibit cancer cell migration/invasion via regulation of urokinase-type plasminogen activator (uPA) signaling. 7 It is also shown to have a role in proper centrosome segregation, and depletion of ECRG2 in cells leads to centrosome amplification, multipolar spindle formation and chromosome aneuploidy.…”

Section: Introductionmentioning

confidence: 99%

Negative regulation of RNA-binding protein HuR by tumor-suppressor ECRG2

2015

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Esophageal cancer-related gene 2 (ECRG2) is a newer tumor suppressor whose function in the regulation of cell growth and apoptosis remains to be elucidated. Here we show that ECRG2 expression was upregulated in response to DNA damage, and increased ECRG2 expression induced growth suppression in cancer cells but not in non-cancerous epithelial cells. ECRG2-mediated growth suppression was associated with activation of caspases and marked reduction in the levels of apoptosis inhibitor, X chromosome-linked inhibitor of apoptosis protein (XIAP). ECRG2, via RNA-binding protein human antigen R (HuR), regulated XIAP mRNA stability and expression. Furthermore, ECRG2 increased HuR ubiquitination and degradation but was unable to modulate the non-ubiquitinable mutant form of HuR. We also identified missense and frame-shift ECRG2 mutations in various human malignancies and noted that, unlike wild-type ECRG2, one cancer-derived ECRG2 mutant harboring glutamic acid instead of valine at position 30 (V30E) failed to induce cell death and activation of caspases. This naturally occurring V30E mutant also did not suppress XIAP and HuR. Importantly, the V30E mutant overexpressing cancer cells acquired resistance against multiple anticancer drugs, thus suggesting that ECRG2 mutations appear to have an important role in the acquisition of anticancer drug resistance in a subset of human malignancies.

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Section: Introductionmentioning

confidence: 99%

Negative regulation of RNA-binding protein HuR by tumor-suppressor ECRG2

2015

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“…Despite increasing understanding of the molecular mechanism of cancers 2, 3, many malignancies remain resistant to established traditional treatments 4, 5. However, the definition of tumor-associated genetic mutations has heightened interest in cancer treatment as the target for gene therapy 6, 7.…”

Section: Introductionmentioning

confidence: 99%

Current Progress in Gene Delivery Technology Based on Chemical Methods and Nano-carriers

Jin¹,

Zeng

Liu³

et al. 2014

Theranostics

351

252

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Gene transfer methods are promising in the field of gene therapy. Current methods for gene transfer include three major groups: viral, physical and chemical methods. This review mainly summarizes development of several types of chemical methods for gene transfer in vitro and in vivo by means of nano-carriers like; calcium phosphates, lipids, and cationic polymers including chitosan, polyethylenimine, polyamidoamine dendrimers, and poly(lactide-co-glycolide). This review also briefly introduces applications of these chemical methods for gene delivery.

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“…ECRG2 mRNA is expressed in esophageal tissue and a number of normal tissues; however, it is significantly downregulated in esophageal cancer tissue and adjacent tissues ( 8 ). ECRG2 has been revealed to inhibit tumor cell growth and proliferation, and promote cell apoptosis in vivo and in vitro ( 9 , 10 , 14 – 15 ). The incidence and progression of tumors results from the abnormal proliferation, differentiation and apoptosis of cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of ECRG2 in combination with cisplatin on the proliferation and apoptosis of EC9706 cells

Song

Deng

Hou

et al. 2014

Experimental and Therapeutic Medicine

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The aim of the present study was to explore the effect of esophageal cancer-related gene 2 (ECRG2) protein in combination with cisplatin (DDP) on the proliferation and apoptosis of esophageal cancer cells. A 3-(4, 5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay was used to examine the effects of ECRG2 alone and ECRG2 in combination with DDP on the proliferation of EC9706 esophageal cancer cells. Hoechst 33258 staining was performed to analyze the effects of ECRG2 alone and ECRG2 in combination with DDP on apoptosis in the EC9706 cells. The expression levels of Bcl-2-associated X protein (Bax) mRNA and protein were determined by reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. The results from the MTT assay revealed that ECRG2 inhibited the proliferation of EC9706 cells and that ECRG2 in combination with DDP had a greater inhibitory effect on cell proliferation. The antiproliferative effects were time- and concentration-dependent, within a certain range of concentrations. The Hoechst 33258 staining results demonstrated that the number of apoptotic cells following treatment with ECRG2 in combination with DDP for 24 h was higher than that following treatment with ECRG2 alone for the same duration. Western blot analysis and RT-PCR results revealed that the expression levels of Bax mRNA and protein were upregulated in cells treated with ECRG2 in combination with DDP compared with those in cells treated with ECRG2 alone. Thus, ECRG2 in combination with DDP had an enhanced inhibitory effect on EC9706 cell proliferation compared with that of ECRG2 alone, and an increased inductive effect on EC9706 cell apoptosis, possibly due to the upregulation of the expression of Bax.

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Suppression of hepatocarcinoma model in vitro and in vivo by ECRG2 delivery using adenoviral vector

Cited by 11 publications

References 14 publications

Negative regulation of RNA-binding protein HuR by tumor-suppressor ECRG2

Negative regulation of RNA-binding protein HuR by tumor-suppressor ECRG2

Current Progress in Gene Delivery Technology Based on Chemical Methods and Nano-carriers

Effect of ECRG2 in combination with cisplatin on the proliferation and apoptosis of EC9706 cells

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