Inhibitory Effects of Syk Transfection on Lung Cancer Cell Invasion

Peng, Chuanliang; Zhang, Ying; Sun, Qifeng; Zhao, Yunpeng; Hao, Yingjie; Zhao, Xiaogang; Cong, Bin

doi:10.7314/apjcp.2013.14.5.3001

Cited by 5 publications

(5 citation statements)

References 11 publications

(9 reference statements)

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“…SYK has previously been identified as putative tumor suppressor gene for NSCLC and suppresses invasive potential in the BRG1-deficient A549 NSCLC cell line (51, 52). IFI16 has also been reported to act as a tumor suppressor but its role in cancer development remains unclear (53-55).…”

Section: Discussionmentioning

confidence: 99%

BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Orvis¹,

et al. 2014

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SWI/SNF chromatin remodeling complexes regulate critical cellular processes including cell cycle control, programmed cell death, differentiation, genomic instability and DNA repair. Inactivation of this class of chromatin remodeling complex has been associated with a variety of malignancies, including lung, ovarian, renal, liver and pediatric cancers. In particular, ~10% of primary human lung non-small lung cancers (NSCLC) display attenuations in the BRG1 ATPase, a core factor in SWI/SNF complexes. To evaluate the role of BRG1 attenuation in NSCLC development, we examined the effect of BRG1 silencing in primary and established human NSCLC cells. BRG1 loss altered cellular morphology and increased tumorigenic potential. Gene expression analyses showed reduced expression of genes known to be associated with progression of human NSCLC. We demonstrated that BRG1 losses in NSCLC cells were associated with variations in chromatin structure, including differences in nucleosome positioning and occupancy surrounding transcriptional start sites of disease-relevant genes. Our results offer direct evidence that BRG1 attenuation contributes to NSCLC aggressiveness by altering nucleosome positioning at a wide range of genes, including key cancer-associated genes.

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Section: Discussionmentioning

confidence: 99%

BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Orvis¹,

et al. 2014

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“…Several clinical studies have indicated that patients with negative SYK expression have a significantly lower overall survival rate compared with patients with positive SYK expression (9–12). Functional studies have demonstrated that dysregulation of SYK is associated with cancer proliferation and metastasis (13–15). These data implicate SYK as a putative tumor suppressor in cancer.…”

Section: Introductionmentioning

confidence: 99%

Alternative splicing of spleen tyrosine kinase differentially regulates colorectal cancer progression

Chen

et al. 2016

Oncology Letters

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Spleen tyrosine kinase (SYK) has been reported as a potential tumor suppressor in colorectal cancer (CRC). However, the role of alternative splicing of SYK in carcinogenesis remains unclear. In the present study, SYK isoforms were overexpressed in the human CRC HCT 116 cell line using lentiviral expression vectors to investigate the biological functions of full length SYK [SYK(L)] and short form SYK [SYK(S)] in CRC. Real-time cellular analysis and the 5-ethynyl-2-deoxyuridine assay were used to detect the effects of SYK(L) and SYK(S) on cell proliferation. Cell cycle progression and migration were assessed via flow cytometry and Transwell assays, respectively. The results revealed that the recombinant lentivirus with SYK(L) overexpression significantly suppressed the proliferation and metastasis of CRC cells, while SYK(S) overexpression did not. In addition, MTS assays demonstrated that SYK(L) and SYK(S) increased the cellular sensitivity to 5-fluorouracil (5-FU), suggesting that SYK(L) and 5-FU produce a significant synergistic effect on CRC cell proliferation, while SYK(S) has an effect on modulating CRC 5-FU sensitivity. Furthermore, quantitative polymerase chain reaction results revealed that SYK(L) was downregulated in 69% of 26 pairs of CRC and adjacent non-cancerous tissues, whereas SYK(S) exhibited no significant differences between tumor and normal tissues. Overall, the present data provides evidence that SYK(L) is a tumor suppressor in CRC, and both SYK(L) and SYK(S) may serve as important predictors in the chemotherapeutic treatment of CRC.

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“…Yet, other studies suggest that Syk is absent from many highly aggressive epithelial cell-derived tumours (Krisenko and Geahlen 2015; Coopman and Mueller 2006) and Syk may increase cell–cell interactions and limit EMT (Krisenko and Geahlen 2015). To be specific, Syk knockdown in more well-differentiated cancers was found to enhance invasive/anchorage-independent growth and motility (Fei et al 2013) whilst its re-introduction in more malignant, invasive cancer cells decreased cancer malignancy through increasing adhesion and reducing tumour cell growth, motility, invasion and metastasis (Ogane et al 2009; Fei et al 2013; Peng et al 2013; Krisenko and Geahlen 2015). The invasion suppressive function of full-length Syk has been reported to correlate with Syk nuclear localisation suggesting that Syk-n possesses biological activities associated with tumour suppression in mammary epithelial cells (Wang et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…A decrease in Syk expression in highly malignant and invasive tumour cells has been observed in a range of cancers including lung (Chuanliang et al 2016) and hepatocellular cancer (Hong et al 2012; Yuan et al 2006). Expression has been found negatively associated with cell proliferation and anchorage-independent growth; moreover, negative associations have also been detected between Syk and cell migration, lymphovascular invasion, microvessel density and/or metastasis formation in cancers (Ogane et al 2009; Fei et al 2013; Nakashima et al 2006; Coopman and Mueller 2006; Peng et al 2013; Chuanliang et al 2016). …”

Section: Introduction and Aimsmentioning

confidence: 99%

Expression of Syk and MAP4 proteins in ovarian cancer

Zhang

Deen

Storr

et al. 2019

J Cancer Res Clin Oncol

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PurposeWe have previously reported on the prognostic importance of the calpain family of proteins in ovarian cancer, especially calpain-2. Spleen tyrosine kinase (Syk) phosphorylates a variety of cytoskeletal proteins with studies suggesting potential interactions between Syk and conventional calpains. Microtubule-associated protein 4 (MAP4) has been reported to be regulated by Syk.MethodsThe current study assessed Syk and MAP4 protein expression, by immunohistochemistry on a tissue microarray comprised of cores from primary ovarian carcinomas (n = 575), to evaluate associations with patient clinical outcomes and other clinicopathological factors and sought to determine whether there were any correlations between the expression of Syk, MAP4 and the calpain system.ResultsMAP4 expression was significantly associated with ovarian cancer histological subtype (P < 0.001), stage (P = 0.001), grade (P < 0.001) and residual tumour (P = 0.005). Despite this finding, we found no significant association existing between MAP4 expression and overall survival. Syk expression was also found significantly associated with histological subtype (P < 0.001). Syk seems to play a contradictory role with respect to tumour progression: low cytoplasmic Syk expression was significantly associated with low stage (P = 0.013), and low nuclear Syk expression with chemo-resistance in patients treated with taxane-containing therapy (P = 0.006). Interestingly, despite the lack of association in the whole cohort, high nuclear Syk expression was significantly associated with better overall survival in certain subgroups (P = 0.001).ConclusionsThe current study indicates a lack of correlation between calpain-2 expression and Syk and MAP4. Syk, MAP4 and calpain-1 appeared to significantly correlate with each other in the whole cohort, with calpain-1 being more highly associated with MAP4 and Syk in mucinous carcinomas. Overall, the current results suggest that Syk, MAP4, and calpain-1 expression are correlated with each other and these proteins may be involved in early stages of tumour spread.Electronic supplementary materialThe online version of this article (10.1007/s00432-019-02856-9) contains supplementary material, which is available to authorized users.

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Inhibitory Effects of Syk Transfection on Lung Cancer Cell Invasion

Cited by 5 publications

References 11 publications

BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Alternative splicing of spleen tyrosine kinase differentially regulates colorectal cancer progression

Expression of Syk and MAP4 proteins in ovarian cancer

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