S100A16 is a prognostic marker for colorectal cancer

Sun, Xu; Wang, Teng; Zhang, Chun; Ning, Kuan; Guan, Zhang-Rui; Chen, Shuxian; Hong, Tang; Hua, Dong

doi:10.1002/jso.24822

Cited by 38 publications

(34 citation statements)

References 48 publications

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“…S100A16 has been found aberrantly expressed in several solid tumours, but its prognostic significance remain controversial. For instance, high S100A16 expression was recognized as a poor prognostic factor in breast, lung and prostate cancer (Saito et al , ; Tanaka et al , ), whereas it was related to better prognosis in OSCC and colorectal cancers (Sapkota et al , ; Sun et al , ). Our study indicated that a higher S100A16 gene expression at diagnosis was correlated with a relatively better RFS and lower CIR in adults with Ph‐negative B‐cell ALL.…”

Section: Discussionmentioning

confidence: 99%

S100A16suppresses the growth and survival of leukaemia cells and correlates with relapse and relapse free survival in adults with Philadelphia chromosome‐negative B‐cell acute lymphoblastic leukaemia

Zhang

et al. 2019

Br J Haematol

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Summary Refinement of risk stratification in Philadelphia chromosome (Ph)‐negative B‐cell acute lymphoblastic leukaemia (ALL) might aid the identification of patients who are likely to relapse. Abnormal S100 calcium binding protein A16 (S100A16) has been implicated in various cancers, but its function remains unclear. We found S100A16 transcript levels were higher in 130 adults with newly‐diagnosed Ph‐negative B‐cell ALL compared with 33 healthy controls. In 115 of 130 patients who achieved first complete remission, those with high S100A16 transcript levels displayed a lower 3‐year cumulative incidence of relapse (CIR; 34% [21, 47%] vs. 40% [48, 72%]; P = 0·012) and higher 3‐year relapse‐free survival (RFS; 65% [53, 78%] vs. 35% [23, 46%]; P = 0·012), especially when receiving chemotherapy only. In multivariate analysis a low S100A16 transcript level was independently‐associated with a higher CIR (Hazard ratio [HR] = 3·74 [1·01–13·82]; P = 0·048) and inferior RFS (HR = 5·78 [1·91, 17·84]; P < 0·001). Function analysis indicated that knockdown of S100A16 promoted proliferation and anti‐apoptosis and reduced chemosensitivity. S100A16 over‐expression revealed an opposite trend, especially in a xeno‐transplant mouse model. Western blotting analysis showed upregulation of PI3K/AKT and ERK1/2 in S100A16‐knockdown and S100A16‐overexpression B‐cell ALL cell lines respectively. Inhibition assays suggested these two signalling pathways participated in the S100A16‐mediated proliferation and survival effects in B‐cell ALL cell lines. Trial Registration: Registered in the Chinese Clinical Trial Registry [ChiCTR‐OCH‐10000940]; http://www.chictr.org.cn.

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Section: Discussionmentioning

confidence: 99%

S100A16suppresses the growth and survival of leukaemia cells and correlates with relapse and relapse free survival in adults with Philadelphia chromosome‐negative B‐cell acute lymphoblastic leukaemia

Zhang

et al. 2019

Br J Haematol

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“…S100A16 is increasingly recognized as an oncogene with multiple roles in tumor onset [10,12]. Recently, researchers found that S100A16 can serve as an effective prognostic indicator for prostate cancer and colorectal cancer, as it is abnormal expressed no matter in cell and tissues, and it is related with the onset and progression of this this disease [9,24]. Further, S100A16 is highly expressed in breast cancer and induced epithelial-mesenchymal transition onset via the Notch1/zinc finger E-box binding homeobox (ZEB) pathway [12].…”

Section: Discussionmentioning

confidence: 99%

S100A16 Regulates HeLa Cell through the Phosphatidylinositol 3 Kinase (PI3K)/AKT Signaling Pathway

Zhang

Yang

et al. 2020

Med Sci Monit

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Background: S100 calcium-binding protein A16 (S100A16) is closely related to the onset and progression of tumors. Material/Methods: In the research, the mainly purpose was to investigate the effect of S100A16 on the proliferation ability, invasion, and angiogenesis of HeLa cells. An adenoviral vector overexpressing S100A16 (Ad-S100A16) was constructed and transfected into HeLa cells, forming a stable cells line of overexpression. The effect of S100A16 on the proliferative capacity of HeLa cells was evaluated by a Cell Counting Kit-8 (CCK-8) assay. Cell migration capacity was determined by a Transwell migration assay. Changes in matrix metalloproteinase-2 (MMP-2), MMP-9, E-cadherin, and vimentin expression were evaluated by a cell-based immunofluorescence assay. The effect of S100A16 on angiogenesis was verified by knockout experiment. Results: Overexpression of S100A16 significantly enhanced the proliferative and migratory capacities of HeLa cells (P<0.05), upregulated expression of matrix MMP-2, MMP-9, vimentin, phosphatidylinositol 3 kinase, and phosphorylated protein kinase B, and downregulated expression of E-cadherin. Vascular endothelial growth factor expression increased, phosphatase and tensin homolog expression decreased, and angiogenesis was positively correlated with S100A16 expression. These effects were largely mediated by the activation of the phosphatidylinositol 3 kinase/protein kinase B pathways. Conclusions: S100A16 could promote the proliferation, migration, and tumor angiogenesis of HeLa cells by regulating the phosphatidylinositol 3 kinase/protein kinase B signaling pathways.

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“…A recent evidence showed that the expression of S100A16 was negatively correlated with the overall survival of bladder cancer patients [50]. Besides breast cancer, S100A16 was identified as an important prognostic marker for colorectal cancer [51] and was shown to be significantly overexpressed in both prostate cancer tissues and cells lines, compared to normal controls [52]. The S100A16 was also upregulated in various types of cancer, including bladder, lung, and pancreatic [53].…”

Section: Discussionmentioning

confidence: 99%

Advancing the Role of Gamma-Tocotrienol as Proteasomes Inhibitor: A Quantitative Proteomic Analysis of MDA-MB-231 Human Breast Cancer Cells

et al. 2019

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Tocotrienol, an analogue of vitamin E has been known for its numerous health benefits and anti-cancer effects. Of the four isoforms of tocotrienols, gamma-tocotrienol (γT3) has been frequently reported for their superior anti-tumorigenic activity in both in vitro and in vivo studies, when compared to its counterparts. In this study, the effect of γT3 treatment in the cytoplasmic and nuclear fraction of MDA-MB-231 human breast cancer cells were assessed using the label-free quantitative proteomics analysis. The cytoplasmic proteome results revealed the ability of γT3 to inhibit a group of proteasome proteins such as PSMA, PSMB, PSMD, and PSME. The inhibition of proteasome proteins is known to induce apoptosis in cancer cells. As such, the findings from this study suggest γT3 as a potential proteasome inhibitor that can overcome deficiencies in growth-inhibitory or pro-apoptotic molecules in breast cancer cells. The nuclear proteome results revealed the involvement of important nuclear protein complexes which hardwire the anti-tumorigenesis mechanism in breast cancer following γT3 treatment. In conclusion, this study uncovered the advancing roles of γT3 as potential proteasomes inhibitor that can be used for the treatment of breast cancer.

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S100A16 is a prognostic marker for colorectal cancer

Abstract: Membrane S100A16 is associated with the prognosis of CRC patients, indicating that S100A16 may be a potential prognostic biomarker and therapeutic target for CRC.

Cited by 38 publications

References 48 publications

S100A16suppresses the growth and survival of leukaemia cells and correlates with relapse and relapse free survival in adults with Philadelphia chromosome‐negative B‐cell acute lymphoblastic leukaemia

S100A16suppresses the growth and survival of leukaemia cells and correlates with relapse and relapse free survival in adults with Philadelphia chromosome‐negative B‐cell acute lymphoblastic leukaemia

S100A16 Regulates HeLa Cell through the Phosphatidylinositol 3 Kinase (PI3K)/AKT Signaling Pathway

Advancing the Role of Gamma-Tocotrienol as Proteasomes Inhibitor: A Quantitative Proteomic Analysis of MDA-MB-231 Human Breast Cancer Cells

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