Downregulation of BTG3 in non-small cell lung cancer

Chen, Xiaobing; Chen, Guoyong; Cao, Xiaoqin; Zhou, Yifeng; Yang, Tiejun; Wei, Sha Xin

doi:10.1016/j.bbrc.2013.06.062

Cited by 18 publications

(17 citation statements)

References 15 publications

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“…These findings suggested that down-regulated BTG3 expression contributed to the malignant transformation of colorectal epithelial cells, consistent with these documents [14, 15, 18, 19]. As reported previously [18], only BTG3b mRNA was found in colorectal cancer and NNM although BTG3 a and 3b were detectable in lung cancer cells and tissues [15].…”

Section: Discussionsupporting

confidence: 90%

“…There appeared BTG3 overexpression in deeply-invasive cancer, while BTG3 overexpression suppressed proliferation, migration, invasion, tumor growth, glycolysis and mitochondrial respiration with the induction of apoptosis or senescence as the reports about gastric cancer [18], and esophageal adenocarcinoma [19] cells. Ectopic BTG3 expression reversed the aggressive behaviors of gastric cancer and hepatocellular cancer cells in vitro [14], and inhibited the tumor growth of lung and gastric cancers in vivo [15, 18]. In contrast, Provenzani et al [21] found that BTG3 mRNA had about 1.83 fold higher in primary than metastatic cancer of colon by cDNA microarray.…”

Section: Discussionmentioning

confidence: 99%

“…BTG3 abrogation might enhance bone morphogenetic protein- induced ectopic bone formation [6] and induce lung carcinogenesis [9]. The down-regulated BTG3 expression was attributable to its promoter methylation in breast, lung, prostate or renal, hepatocellular, and gastric cancer tissues or cells [10–15]. The down- regulated BTG3 expression was also found during ovarian carcinogenesis, and positively correlated with the dedifferentiation, FIGO staging, and adverse prognosis of cancers [16].…”

Section: Introductionmentioning

confidence: 99%

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The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: Anin vitroandvivostudy

Zheng

et al. 2017

Oncotarget

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Here, we found that down-regulated expression of BTG3 might be positively correlated with colorectal carcinogenesis and its overexpression suppressed proliferation, glycolysis, mitochondrial respiration, cell cycle progression, migration, and invasion, and induced apoptosis, senescence and differentiation in SW480 and SW620 cells. After treated with cisplatin, MG132, paclitaxel and SAHA, BTG3 transfectants exhibited lower viability and higher apoptosis than the control in both time- and dose-dependent manners. BTG3 overexpression up- regulated the protein expression of Cyclin E, p16, p27, NF-κB, p38α/β, XIAP, Bcl-2, ATG14 and p53, but down-regulated the mRNA expression of MRP1, BCRP, and mTOR in SW480 and SW620 cells. BTG3 overexpression inhibited tumor growth of SW620 cells by suppressing proliferation and inducing apoptosis. It was suggested that down-regulated BTG3 expression might be considered as a marker for colorectal carcinogenesis. BTG3 overexpression might reverse the aggressive phenotypes and be employed as a potential target for gene therapy of colorectal cancer.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: Anin vitroandvivostudy

Zheng

et al. 2017

Oncotarget

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“…Recently, several studies have shown that BTG3 was associated with tumorigenesis. It has been reported as a tumor suppressor in several tumor types (Majid et al 2009(Majid et al , 2010Yu et al 2008;Lv et al 2013;Chen et al 2013). However, the expression pattern and function of BTG3 in the progression of GC remain elusive.…”

Section: Discussionmentioning

confidence: 96%

Down-regulation of BTG3 promotes cell proliferation, migration and invasion and predicts survival in gastric cancer

Ren

Zhu

et al. 2014

J Cancer Res Clin Oncol

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“…BTG3 has previously been reported to be downregulated in a wide variety of breast cancer cell lines (Yu et al, 2008 ) and belongs to a protein family characterized by its antiproliferative properties. Moreover, the low expression of BTG3 has previously been related to the progression of several kinds of cancer, such as adenocarcinoma, oral squamous cell cancer, non-small cell lung cancer, prostate cancer, and hepatocellular carcinoma (Chen et al, 2013 ; Lv et al, 2013 ). Additionally, the downregulation of BTG3 is a feature of breast cancer patient samples in the study from Liu et al ( 2011 ).…”

Section: Resultsmentioning

confidence: 99%

A genomic approach to study down syndrome and cancer inverse comorbidity: untangling the chromosome 21

et al. 2015

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Down syndrome (DS), one of the most common birth defects and the most widespread genetic cause of intellectual disabilities, is caused by extra genetic material on chromosome 21 (HSA21). The increased genomic dosage of trisomy 21 is thought to be responsible for the distinct DS phenotypes, including an increased risk of developing some types of childhood leukemia and germ cell tumors. Patients with DS, however, have a strikingly lower incidence of many other solid tumors. We hypothesized that the third copy of genes located in HSA21 may have an important role on the protective effect that DS patients show against most types of solid tumors. Focusing on Copy Number Variation (CNV) array data, we have generated frequencies of deleted regions in HSA21 in four different tumor types from which DS patients have been reported to be protected. We describe three different regions of deletion pointing to a set of candidate genes that could explain the inverse comorbidity phenomenon between DS and solid tumors. In particular we found RCAN1 gene in Wilms tumors and a miRNA cluster containing miR-99A, miR-125B2 and miR-LET7C in lung, breast, and melanoma tumors as the main candidates for explaining the inverse comorbidity observed between solid tumors and DS.

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Downregulation of BTG3 in non-small cell lung cancer

Cited by 18 publications

References 15 publications

The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: Anin vitroandvivostudy

The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: Anin vitroandvivostudy

Down-regulation of BTG3 promotes cell proliferation, migration and invasion and predicts survival in gastric cancer

A genomic approach to study down syndrome and cancer inverse comorbidity: untangling the chromosome 21

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