Suppressing the growth of rectal cancer xenografts derived from patient tumors by an adenovector expressing small hairpin RNA targeting Bcl‐XL

Zhu, Hongbo; Zhou, Wei; Hu, Jingzi; Huang, Zhi‐Zhen; Lao, Weifeng; Huang, Xuefeng; He, Chao

doi:10.1002/jgm.2681

Cited by 4 publications

(3 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Deregulation of apoptosis during tumor development can be caused by a disturbance in the homeostatic balance of the Bcl-2 family members [16]. Specially, Bcl-XL is overexpressed in colorectal cancers and knockdown of this protein could suppress the growth of rectal cancer xenografts derived from patient tumors [17]. In addition, it has been reported that Bax/Bcl-2 ratio is considered as a prognostic marker with age and tumor location in colorectal cancer [18].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-203-mediated posttranscriptional deregulation of CPEB4 contributes to colorectal cancer progression

Zhong

Xiao

Chen

et al. 2015

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

MicroRNA-203-mediated posttranscriptional deregulation of CPEB4 contributes to colorectal cancer progression

Zhong

Xiao

Chen

et al. 2015

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

“…They reported the loss of human stromal cells after engraftment, observed a metastatic phenotype in some models, and finally compared the molecular profile with the drug sensitivity of each tumor model. In colorectal cancer, PDX model has also been used to report a suppression of the growth of tumors by an adenovector expressing small hairpin RNA targeting Bcl-XL [52]. The result showed that Ad/Bcl-XL shRNA with or without 5-Fu has effective anti-tumor effects on the patient tumor-derived rectal cancer xenografts.…”

Section: Pdx In Colorectal Cancermentioning

confidence: 99%

Evolution of Tumor Model: From Animal Model of Tumor to Tumor Model in Animal

Dey¹,

Sun²,

Leyland-Jones³

et al. 2013

JCT

View full text Add to dashboard Cite

Patient derived xenograft (PDX) is defined as a growth of patients' tumor in the xenograft setting. The evolution of cancer model in animal has a century old history. The most single reason that exerted the pressure on the traditional animal model of cancer to evolve to PDX is that the traditional models have not delivered as expected and traditional models have not predicted clinical success. In spite of well above 50 drugs developed and approved for oncology over the last several decades, there remains a nirking paucity of clinical success as a reminder that this war on cancer riding on the animal model is far from won. In a backbreaking attempt to analyze the failure, the limitation of the "model" system appeared to be the most rational cause of this shortcoming. It was more of a failure to test a drug rather than a failure to make a drug that stunted our collective growth and success in cancer research. PDX is the product of this age-old failure and its fitness is currently tested in virtually all organ-type solid tumors. This review will present and appraise PDX model in the context of its evolution, its future promise, its limitations and more specifically, the current content of PDX in different solid tumors including breast, lung, colorectal, prostrate, GBM, pancreatic, hepatocellular carcinoma and melanoma.

show abstract

“…It remains a priority to identify potential biomarkers that could predict recurrence, DFS and OS. Moreover, no insight into the molecular events responsible for tumor proliferation, invasion and other malignant biological properties was given by the majority of prognostic factors .…”

Section: Introductionmentioning

confidence: 99%

Lentivirus‐mediated shRNA interference of ghrelin receptor blocks proliferation in the colorectal cancer cells

Huang

et al. 2016

Cancer Medicine

View full text Add to dashboard Cite

Ghrelin, an orexigenic peptide, acts via the growth hormone secretagogue receptor (GHSR) to stimulate the release of growth hormone. Moreover, it has a range of biological actions, including the stimulation of food intake, modulation of insulin signaling and cardiovascular effects. Recently, it has been demonstrated that ghrelin has a proliferative and antiapoptotic effects in cancers, suggesting a potential role in promoting tumor growth. However, it remains unknown whether GHSR contributes to colorectal cancer proliferation. In this study, the therapeutic effect of lentivirus‐mediated short hairpin RNA (shRNA) targeting ghrelin receptor 1a (GHSR1a) was analyzed in colorectal cancer cell line SW480 both in vitro and in vivo. Our study demonstrated that ghrelin and GHSR1a are significantly upregulated in cancerous colorectal tissue samples and cell lines. In vitro, human colorectal cancer cell line SW480 with downregulation of GHSR1a by shRNA showed significant inhibition of cell viability compared with blank control (BC) or scrambled control (SC) regardless of the application of exogenous ghrelin. Furthermore, GHSR1a silencing by target specific shRNA was shown capable of increasing PTEN, inhibiting AKT phosphorylation and promoting the release of p53 in SW480 cells. In addition, the effects of GHSR1a knockdown were further explored in vivo using colorectal tumor xenograft mouse model. The tumor weights were decreased markedly in GHSR1α knockdown SW480 mouse xenograft tumors compared with blank control or negative control tumors. Our results suggested that the expression of GHSR1a is significantly correlated with the growth of colorectal cancer cells, and the GHSR1a knockdown approach may be a potential therapy for the treatment of colorectal cancer.

show abstract

Suppressing the growth of rectal cancer xenografts derived from patient tumors by an adenovector expressing small hairpin RNA targeting Bcl‐XL

Abstract: These data indicate that Ad/Bcl-XL shRNA with or without 5-Fu has effective anti-tumor effects on the patient tumor-derived rectal cancer xenografts, suggesting that it could be a potential strategy for rectal cancer therapy.

Cited by 4 publications

References 21 publications

MicroRNA-203-mediated posttranscriptional deregulation of CPEB4 contributes to colorectal cancer progression

MicroRNA-203-mediated posttranscriptional deregulation of CPEB4 contributes to colorectal cancer progression

Evolution of Tumor Model: From Animal Model of Tumor to Tumor Model in Animal

Lentivirus‐mediated shRNA interference of ghrelin receptor blocks proliferation in the colorectal cancer cells

Contact Info

Product

Resources

About