Prognostic values of S100 family members in ovarian cancer patients

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Objective

Exhibiting high consistence in sequence and structure, S100 family members are interchangeable in function and they show a wide spectrum of biological processes, including proliferation, apoptosis, migration, inflammation and differentiation and the like. While the prognostic value of each individual S100 in ovarian cancer is still elusive. In current study, we investigated the prognostic value of S100 family members in the ovarian cancer.

Methods

We used the Kaplan Meier plotter (KM plotter) database, in which updated gene expression data and survival information are from 1657 ovarian cancer patients, to assess the relevance of individual S100 family mRNA expression to overall survival in various ovarian cancer subtypes and different clinicopathological features.

Results

It was found that high expression of S100A2 (HR = 1.18, 95%CI: 1.04–1.34, P = 0.012), S100A7A (HR = 1.3, 95%CI: 1.04–1.63, P = 0.02),S100A10 (HR = 1.2, 95%CI: 1.05–1.38, P = 0.0087),and S100A16 (HR = 1.23, 95%CI: 1–1.51, P = 0.052) were significantly correlated with worse OS in all ovarian cancer patients, while the expression of S100A1 (HR = 0.87, 95%CI: 0.77–0.99, P = 0.039), S100A3 (HR = 0.83, 95%CI: 0.71–0.96, P = 0.0011), S100A5 (HR = 0.84, 95%CI: 0.73–0.97, P = 0.017), S100A6 (HR = 0.84, 95%CI: 0.72–0.98, P = 0.024), S100A13 (HR = 0.85, 95%CI:0.75–0.97, P = 0.014) and S100G (HR = 0.86, 95%CI: 0.74–0.99, P = 0.041) were associated with better prognosis. Furthermore, we assessed the prognostic value of S100 expression in different subtypes and the clinicopathological features, including pathological grades, clinical stages and TP53 mutation status, of ovarian cancer patients.

Conclusion

Comprehensive understanding of the S100 family members may have guiding significance for the diagnosis and outcome of ovarian cancer patients.

Electronic supplementary material

The online version of this article (10.1186/s12885-018-5170-3) contains supplementary material, which is available to authorized users.

Related collections

Most cited references 77

Record: found
Abstract: found
Article: not found

S100 proteins in cancer.

Anne Bresnick, David Weber, Danna B Zimmer (2015)

In humans, the S100 protein family is composed of 21 members that exhibit a high degree of structural similarity, but are not functionally interchangeable. This family of proteins modulates cellular responses by functioning both as intracellular Ca(2+) sensors and as extracellular factors. Dysregulated expression of multiple members of the S100 family is a common feature of human cancers, with each type of cancer showing a unique S100 protein profile or signature. Emerging in vivo evidence indicates that the biology of most S100 proteins is complex and multifactorial, and that these proteins actively contribute to tumorigenic processes such as cell proliferation, metastasis, angiogenesis and immune evasion. Drug discovery efforts have identified leads for inhibiting several S100 family members, and two of the identified inhibitors have progressed to clinical trials in patients with cancer. This Review highlights new findings regarding the role of S100 family members in cancer diagnosis and treatment, the contribution of S100 signalling to tumour biology, and the discovery and development of S100 inhibitors for treating cancer.

0 comments Cited 360 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: found

Is Open Access

Inhibition of dendritic cell differentiation and accumulation of myeloid-derived suppressor cells in cancer is regulated by S100A9 protein

Pingyan Cheng, Cesar A. Corzo, Noreen Luetteke … (2008)

Accumulation of myeloid-derived suppressor cells (MDSCs) associated with inhibition of dendritic cell (DC) differentiation is one of the major immunological abnormalities in cancer and leads to suppression of antitumor immune responses. The molecular mechanism of this phenomenon remains unclear. We report here that STAT3-inducible up-regulation of the myeloid-related protein S100A9 enhances MDSC production in cancer. Mice lacking this protein mounted potent antitumor immune responses and rejected implanted tumors. This effect was reversed by administration of wild-type MDSCs from tumor-bearing mice to S100A9-null mice. Overexpression of S100A9 in cultured embryonic stem cells or transgenic mice inhibited the differentiation of DCs and macrophages and induced accumulation of MDSCs. This study demonstrates that tumor-induced up-regulation of S100A9 protein is critically important for accumulation of MDSCs and reveals a novel molecular mechanism of immunological abnormalities in cancer.

0 comments Cited 288 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

S100A8 and S100A9 in inflammation and cancer.

Christoffer Gebhardt, Julia Németh, Peter Angel … (2006)

Calprotectin (S100A8/A9), a heterodimer of the two calcium-binding proteins S100A8 and S100A9, was originally discovered as immunogenic protein expressed and secreted by neutrophils. Subsequently, it has emerged as important pro-inflammatory mediator in acute and chronic inflammation. More recently, increased S100A8 and S100A9 levels were also detected in various human cancers, presenting abundant expression in neoplastic tumor cells as well as infiltrating immune cells. Although, many possible functions have been proposed for S100A8/A9, its biological role still remains to be defined. Altogether, its expression and potential cytokine-like function in inflammation and in cancer suggests that S100A8/A9 may play a key role in inflammation-associated cancer.

0 comments Cited 242 times – based on 0 reviews      Review now

All references

Author and article information

Contributors

Yang Bai: baiyangbaiyangby@163.com

Liang-Dong Li: lild0123@163.com

Jun Li: fdlijun2008@163.com

Xin Lu: 052108365@fudan.edu.cn

Journal

Journal ID (nlm-ta): BMC Cancer

Journal ID (iso-abbrev): BMC Cancer

Title: BMC Cancer

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2407

Publication date (Electronic): 17 December 2018

Publication date PMC-release: 17 December 2018

Publication date Collection: 2018

Volume: 18

Electronic Location Identifier: 1256

Affiliations

[1 ]ISNI 0000 0001 0125 2443, GRID grid.8547.e, Obstetrics and Gynecology Hospital, , Fudan University, ; Shanghai, 200011 China

[2 ]ISNI 0000 0001 0125 2443, GRID grid.8547.e, Department of Obstetrics and Gynecology of Shanghai Medical College, , Fudan University, ; Shanghai, 200032 China

[3 ]Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, 200011 China

[4 ]ISNI 0000 0004 1808 0942, GRID grid.452404.3, Department of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, , Fudan University Shanghai Cancer Center, ; Shanghai, 200030 China

[5 ]ISNI 0000 0001 0125 2443, GRID grid.8547.e, Department of Oncology, Shanghai Medical College, , Fudan University, ; Shanghai, 200030 China

[6 ]ISNI 0000 0004 1755 1415, GRID grid.412312.7, Present Address: Department of Gynecology, , Obstetrics and Gynecology Hospital of Fudan University, ; No.419, Fangxie Road, Shanghai, 200011 China

Article

Publisher ID: 5170

DOI: 10.1186/s12885-018-5170-3

PMC ID: 6296138

PubMed ID: 30558666

SO-VID: 24a6edd1-5fb3-4821-a413-9407427cb5c9

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 31 May 2018

Date accepted : 2 December 2018

Funding

Funded by: Natural Science Foundation of China

Award ID: 17ZR1403500

Funded by: Shanghai Sailing Program grants awarded

Award ID: 16YF1401100

Award Recipient : Jun Li

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: prognosis,ovarian cancer,s100 family,kaplan meier plotter

Data availability:

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: prognosis, ovarian cancer, s100 family, kaplan meier plotter

Comments

Comment on this article

Cited by 27

See all cited by

Most referenced authors 929

See all reference authors

- Version 1