hSav1 interacts with HAX1 and attenuates its anti-apoptotic effects in MCF-7 breast cancer cells

Luo, Xuelai; Li, Zhaoming; Li, Xiaolan; Wang, Guihua; Liu, Weicheng; Dong, Suo; Cai, Shaoxin; Tao, Deding; Yan, Qun; Wang, Jing; Leng, Yan; Gong, Jianping; Hu, Junbo

doi:10.3892/ijmm.2011.692

Cited by 17 publications

(14 citation statements)

References 27 publications

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“…Oncomine Cancer Microarray database [25] (http://www.oncomine.org) were used to study gene expression of Six1 in human pancreatic cancer samples as we previously described [26]. Gene expression data were also obtained from NCBI Gene Expression Omnibus (GEO) database (accession numbers GSE15471, GSE32676 and GSE28735; http://www.ncbi.nlm.nih.gov/geo) [27]–[29].…”

Section: Methodsmentioning

confidence: 99%

Six1 Promotes Proliferation of Pancreatic Cancer Cells via Upregulation of Cyclin D1 Expression

Tian

et al. 2013

PLoS ONE

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Six1 is one of the transcription factors that act as master regulators of development and are frequently dysregulated in cancers. However, the role of Six1 in pancreatic cancer is not clear. Here we show that the relative expression of Six1 mRNA is increased in pancreatic cancer and correlated with advanced tumor stage. In vitro functional assays demonstrate that forced overexpression of Six1 significantly enhances the growth rate and proliferation ability of pancreatic cancer cells. Knockdown of endogenous Six1 decreases the proliferation of these cells dramatically. Furthermore, Six1 promotes the growth of pancreatic cancer cells in a xenograft assay. We also show that the gene encoding cyclin D1 is a direct transcriptional target of Six1 in pancreatic cancer cells. Overexpression of Six1 upregulates cyclin D1 mRNA and protein, and significantly enhances the activity of the cyclin D1 promoter in PANC-1 cells. We demonstrate that Six1 promotes cell cycle progression and proliferation by upregulation of cyclin D1. These data suggest that Six1 is overexpressed in pancreatic cancer and may contribute to the increased cell proliferation through upregulation of cyclin D1.

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Section: Methodsmentioning

confidence: 99%

Six1 Promotes Proliferation of Pancreatic Cancer Cells via Upregulation of Cyclin D1 Expression

Tian

et al. 2013

PLoS ONE

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“…Western blot analyses were performed as previously described (21). For immunoblotting of LC3 in SH-SY5Y cells, mycoplasma-infected (infected at the MOI ratio of 10:1 for 24 h) cells and control SH-SY5Y cells were serum starved for 2 h prior to treatment with 0.1% dimethylsulfoxide (DMSO) or Bafilomycin A1 (Baf A1; 10 nM) for 4 h; and lysates were collected for western blot analysis against LC3.…”

Section: Methodsmentioning

confidence: 99%

Synergism between upregulation of Rab7 and inhibition of autophagic degradation caused by mycoplasma facilitates intracellular mycoplasma infection

Zhou

et al. 2014

Molecular Medicine Reports

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Following fusion of a mycoplasma with a host cell membrane, the inserted components of mycoplasma may then be transported through the endocytic pathway. However, the effects of mycoplasmas on the host cell endomembrane system are largely unknown. In this study, mycoplasma-induced changes in the dynamics of endocytic and autophagic systems were investigated. Endocytosis and autophagy are two major processes involved in the survival of intracellular prokaryotic pathogens. It was found that, immediately following infection, mycoplasmas induce endocytosis in the host cell; however, in the long term the mycoplasmas suppress turnover of the components of the endocytic pathway. Immunofluorescence microscopy revealed that Rab7 and LC3-II are recruited to the intracellular mycoplasma-containing compartments. Western blot analysis and quantitative reverse transcription-polymerase chain reaction (qPCR) showed that mycoplasmas increase expression of Rab7 by upregulating transcription, but increase levels of LC3-II and p62 by post-translational regulation. Furthermore, it was demonstrated that mycoplasma infection causes inhibition of autophagic degradation of LC3-II and p62. In addition, it was found that upregulation of Rab7 and inhibition of autophagic degradation synergistically contributes to intracellular mycoplasma accumulation. In conclusion, these findings suggest that mycoplasmas may manipulate host cell endosomal and autophagic systems in order to facilitate intracellular infection.

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“…In our previous study, yeast two-hybrid screening demonstrated that HAX-1 had a key role in the Salvador-warts-hippo signaling pathway, which is an important supplement for the classic apoptosis pathway ( 16 , 17 ). The present study aimed to analyze the potential prognostic significance of HAX-1 in CRC by detecting its expression levels in human colorectal tumor tissues, and to assess the role of HAX-1 in apoptosis and proliferation using gene-overexpression and silencing methods.…”

Section: Introductionmentioning

confidence: 99%

Expression of HAX-1 in colorectal cancer and its role in cancer cell growth

Jiang

Yang

et al. 2015

Molecular Medicine Reports

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Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Hematopoietic cell-specific protein 1-associated protein X-1 (HAX-1) has been found to be involved in several types of cancer. However, the role of HAX-1 in CRC remains to be elucidated. The aim of the present study was to investigate whether the expression of HAX-1 is associated with the progression of CRC, and to determine the effects of HAX-1 on the apoptosis and proliferation of CRC cells. Tumor tissues and adjacent noncancerous tissues were collected from 60 patients with CRC, following the provision of informed consent. The expression levels of HAX-1 and the association with clinical and pathological characteristics were then analyzed. The expression levels of HAX-1 were significantly higher in the cancerous tissues from the patients with CRC, particularly in tissues of an advanced stage of cancer. In addition, HAX-1 expression was associated with malignant progression and poor prognosis. Furthermore, SW480 CRC cells, overexpressing HAX-1, exhibited increased resistance to camptothecin in vitro, and promoted proliferation in vitro and in vivo. By contrast, HAX-1 knockdown significantly decreased the proliferation. In addition, the expression levels of ki-67 and phosphorylatedakt were inhibited following HAX-1 knockdown. In conclusion, the expression levels of HAX-1 were increased in cancerous tissue from patients with CRC, and were associated with progression of the disease. These results suggested that HAX-1 may contribute to chemotherapy resistance and malignant progression in CRC.

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hSav1 interacts with HAX1 and attenuates its anti-apoptotic effects in MCF-7 breast cancer cells

Cited by 17 publications

References 27 publications

Six1 Promotes Proliferation of Pancreatic Cancer Cells via Upregulation of Cyclin D1 Expression

Six1 Promotes Proliferation of Pancreatic Cancer Cells via Upregulation of Cyclin D1 Expression

Synergism between upregulation of Rab7 and inhibition of autophagic degradation caused by mycoplasma facilitates intracellular mycoplasma infection

Expression of HAX-1 in colorectal cancer and its role in cancer cell growth

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