Differential gene expression identified in Uigur women cervical squamous cell carcinoma by suppression subtractive hybridization

Pan, Zhijuan; Chen, S; X, Pan; Z, Wang; Han, Haitang; Zheng, Wenjing; Wang, X; F, Li; Qu, S.; Shao, Renfu

doi:10.4149/neo_2010_02_123

Cited by 34 publications

(27 citation statements)

References 15 publications

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“…IFITM1 expression has been linked to the progression of several aggressive cancer types, including cancers of the cervix, esophagus, colon, ovary and brain [9, 25, 39, 52, 55, 64, 77]. The mechanism by which IFITM1 promotes tumor progression is not understood, however, IFITM1 is known to play a role in DNA damage resistance which contributes to treatment failure in cancer [12, 72, 78].…”

Section: Discussionmentioning

confidence: 99%

IFITM1 suppression blocks proliferation and invasion of aromatase inhibitor-resistant breast cancer in vivo by JAK/STAT-mediated induction of p21

et al. 2017

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Interferon induced transmembrane protein 1 (IFITM1) belongs to a family of interferon stimulated genes (ISGs) that is associated with tumor progression and DNA damage resistance, however, its role in endocrine resistance is not known. Here, we correlate IFITM1 expression with clinical stage and poor response to endocrine therapy in a tissue microarray consisting of 94 estrogen receptor (ER)-positive breast tumors. IFITM1 overexpression is confirmed in the AI-resistant MCF-7:5C cell line and not found in AI-sensitive MCF-7 cells. In this study, the orthotopic (mammary fat pad) and mouse mammary intraductal (MIND) models of breast cancer are used to assess tumor growth and invasion in vivo. Lentivirus-mediated shRNA knockdown of IFITM1 in AI-resistant MCF-7:5C cells diminished tumor growth and invasion and induced cell death, whereas, overexpression of IFITM1 in wild-type MCF-7 cells promoted estrogen-independent growth and enhanced their aggressive phenotype. Mechanistic studies indicated that loss of IFITM1 in MCF-7:5C cells markedly increased p21 transcription, expression and nuclear localization which was mediated by JAK/STAT activation. These findings suggest IFITM1 overexpression contributes to breast cancer progression and that targeting IFITM1 may be therapeutically beneficial to patients with endocrine-resistant disease.

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Section: Discussionmentioning

confidence: 99%

IFITM1 suppression blocks proliferation and invasion of aromatase inhibitor-resistant breast cancer in vivo by JAK/STAT-mediated induction of p21

et al. 2017

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“…Nevertheless, recent IFITM1 expression data in different cancer types have led us to hypothesize that it might possess oncogenic function; for instance, IFITM1 expression has been found to be greatly elevated in colon cancer [11], cervical cancer [12], esophageal cancer [13], ovarian cancer, and mouse astrocytoma [10, 14]. In this study, we determined IFITM1 expression levels in five human glioma cell lines and investigated its roles in proliferation, migration, and invasion glioma cells.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of interferon-induced transmembrane protein 1 (IFITM1) inhibits proliferation, migration, and invasion of glioma cells

Chow

et al. 2010

J Neurooncol

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Interferon-induced transmembrane protein 1 (IFITM1) has recently been identified as a new molecular marker in human colorectal cancer. However, its role in glioma carcinogenesis is not known. In this study, we demonstrated that suppression of IFITM1 expression significantly inhibited proliferation of glioma cells in a time-dependent manner. The growth inhibitory effect was mediated by cell cycle arrest. Furthermore, IFITM1 knockdown significantly inhibited migration and invasion of glioma cells, which could be attributed to decreased expression and enzymatic activity of matrix metalloproteinase 9. Taken together, these results suggest that IFITM1 is a potential therapeutic target for gliomas.

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“…IFITM1 is implicated in IFNγ mediated growth control in some cancer cells with an active p53 pathway [35]. IFITM1 is also implicated in a growth stimulatory role in cervical squamous cancers [36] [37]. The HPV16+ and IFITM1/3 positive cervical cancer cell line SiHa [38] [39] exhibit IFNγ inducible STAT1, IRF1, and IFITM1/3 proteins ( Fig.…”

Section: Developing An Ifitm1 and Ifitm3 Double Null Cell Line Using mentioning

confidence: 99%

The effects of IFITM1 and IFITM3 gene deletion on IFNγ stimulated protein synthesis

Gómez-Herranz

Nekulova

Faktor

et al. 2019

Cellular Signalling

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A B S T R A C TInterferon-induced transmembrane proteins IFITM1 and IFITM3 (IFITM1/3) play a role in both RNA viral restriction and in human cancer progression. Using immunohistochemical staining of FFPE tissue, we identified subgroups of cervical cancer patients where IFITM1/3 protein expression is inversely related to metastasis. Guide RNA-CAS9 methods were used to develop an isogenic IFITM1/IFITM3 double null cervical cancer model in order to define dominant pathways triggered by presence or absence of IFITM1/3 signalling. A pulse SILAC methodology identified IRF1, HLA-B, and ISG15 as the most dominating IFNγ inducible proteins whose synthesis was attenuated in the IFITM1/IFITM3 double-null cells. Conversely, SWATH-IP mass spectrometry of ectopically expressed SBP-tagged IFITM1 identified ISG15 and HLA-B as dominant co-associated proteins. ISG15ylation was attenuated in IFNγ treated IFITM1/IFITM3 double-null cells. Proximity ligation assays indicated that HLA-B can interact with IFITM1/3 proteins in parental SiHa cells. Cell surface expression of HLA-B was attenuated in IFNγ treated IFITM1/IFITM3 double-null cells. SWATH-MS proteomic screens in cells treated with IFITM1-targeted siRNA cells resulted in the attenuation of an interferon regulated protein subpopulation including MHC Class I molecules as well as IFITM3, STAT1, B2M, and ISG15. These data have implications for the function of IFITM1/3 in mediating IFNγ stimulated protein synthesis including ISG15ylation and MHC Class I production in cancer cells. The data together suggest that pro-metastatic growth associated with IFITM1/3 negative cervical cancers relates to attenuated expression of MHC Class I molecules that would support tumor immune escape.Abbreviations: B2M, beta-2-microglobulin; FASP, filter-aided sample preparation; FA, formic acid; HLA, human leucocyte antigen; IFN, interferon; IFITM1/3, interferon-induced transmembrane receptors 1 and 3; ISG15, interferon-stimulated gene 15; IRF1, interferon regulatory factor 1; MHC, major histocompatibility complex; MS, mass spectrometry; NMWCO, nominal molecular weight cut-off; PBS, phosphate-buffered saline; PLA, proximity ligation assay; RT, room temperature; SWATH-IP, SWATH immunoprecipitation; SBP, twin streptavidin binding protein; UPLC, ultra performance liquid chromatography ⁎ Corresponding authors at

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Differential gene expression identified in Uigur women cervical squamous cell carcinoma by suppression subtractive hybridization

Cited by 34 publications

References 15 publications

IFITM1 suppression blocks proliferation and invasion of aromatase inhibitor-resistant breast cancer in vivo by JAK/STAT-mediated induction of p21

IFITM1 suppression blocks proliferation and invasion of aromatase inhibitor-resistant breast cancer in vivo by JAK/STAT-mediated induction of p21

Knockdown of interferon-induced transmembrane protein 1 (IFITM1) inhibits proliferation, migration, and invasion of glioma cells

The effects of IFITM1 and IFITM3 gene deletion on IFNγ stimulated protein synthesis

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