Skip to main content

S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer

Publication ,  Journal Article
Chen, H; Ma, J; Sunkel, B; Luo, A; Ding, F; Li, Y; He, H; Zhang, S; Xu, C; Jin, Q; Wang, Q; Liu, Z
Published in: Molecular Cancer Research
December 1, 2013

Aberrant keratinocyte differentiation is a key mechanism in the initiation of cancer. Because activities regulating differentiation exhibit altered or reduced capacity in esophageal cancer cells, it is vital to pinpoint those genes that control epidermal proliferation and terminal differentiation to better understand esophageal carcinogenesis. S100A14 is a member of the S100 calcium-binding protein family and has been suggested to be involved in cell proliferation, apoptosis, and invasion. The present study used immunohistochemistry analysis of S100A14 in clinical specimens of esophageal squamous cell carcinoma (ESCC) to show that decreased S100A14 is strongly correlated with poor differentiation. Furthermore, both mRNA and protein expression of S100A14 was drastically increased upon 12-O-tetra-decanoylphorbol-13-acetate (TPA) and calcium-induced esophageal cancer cell differentiation. Overexpression of S100A14 resulted in a G1-phase cell cycle arrest and promoted calcium-inhibited cell growth. Conversely, decreasing S100A14 expression significantly promoted G1–S transition and prevented the morphologic changes associated with calcium-induced cell differentiation. Molecular investigation demonstrated that S100A14 altered the calcium-induced expression of late markers of differentiation, with the most prominent effect on involucrin (IVL) and filaggrin (FLG). Finally, it was determined that S100A14 is transcriptionally regulated by JunB and that S100A14 and JunB status significantly correlated in ESCC tissue. In summary, these data demonstrate that S100A14 is transcriptionally regulated by JunB and involved in ESCC cell differentiation.Implications: This study further differentiates the molecular mechanism controlling the development and progression of esophageal cancer. Mol Cancer Res; 11(12); 1542–53. ©2013 AACR.

Duke Scholars

Published In

Molecular Cancer Research

DOI

EISSN

1557-3125

ISSN

1541-7786

Publication Date

December 1, 2013

Volume

11

Issue

12

Start / End Page

1542 / 1553

Publisher

American Association for Cancer Research (AACR)

Related Subject Headings

  • Oncology & Carcinogenesis
  • Developmental Biology
  • 1112 Oncology and Carcinogenesis
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Chen, H., Ma, J., Sunkel, B., Luo, A., Ding, F., Li, Y., … Liu, Z. (2013). S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer. Molecular Cancer Research, 11(12), 1542–1553. https://doi.org/10.1158/1541-7786.mcr-13-0317
Chen, Hongyan, Jianlin Ma, Benjamin Sunkel, Aiping Luo, Fang Ding, Yi Li, Huan He, et al. “S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer.” Molecular Cancer Research 11, no. 12 (December 1, 2013): 1542–53. https://doi.org/10.1158/1541-7786.mcr-13-0317.
Chen H, Ma J, Sunkel B, Luo A, Ding F, Li Y, et al. S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer. Molecular Cancer Research. 2013 Dec 1;11(12):1542–53.
Chen, Hongyan, et al. “S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer.” Molecular Cancer Research, vol. 11, no. 12, American Association for Cancer Research (AACR), Dec. 2013, pp. 1542–53. Crossref, doi:10.1158/1541-7786.mcr-13-0317.
Chen H, Ma J, Sunkel B, Luo A, Ding F, Li Y, He H, Zhang S, Xu C, Jin Q, Wang Q, Liu Z. S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer. Molecular Cancer Research. American Association for Cancer Research (AACR); 2013 Dec 1;11(12):1542–1553.

Published In

Molecular Cancer Research

DOI

EISSN

1557-3125

ISSN

1541-7786

Publication Date

December 1, 2013

Volume

11

Issue

12

Start / End Page

1542 / 1553

Publisher

American Association for Cancer Research (AACR)

Related Subject Headings

  • Oncology & Carcinogenesis
  • Developmental Biology
  • 1112 Oncology and Carcinogenesis