Preprint Review Version 1 This version is not peer-reviewed

S100A10 in Cancer Progression and Chemotherapy Resistance: A Novel Therapeutic Target against Ovarian Cancer

Version 1 : Received: 15 October 2018 / Approved: 15 October 2018 / Online: 15 October 2018 (14:02:03 CEST)

A peer-reviewed article of this Preprint also exists.

Noye, T.M.; Lokman, N.A.; Oehler, M.K.; Ricciardelli, C. S100A10 and Cancer Hallmarks: Structure, Functions, and its Emerging Role in Ovarian Cancer. Int. J. Mol. Sci. 2018, 19, 4122. Noye, T.M.; Lokman, N.A.; Oehler, M.K.; Ricciardelli, C. S100A10 and Cancer Hallmarks: Structure, Functions, and its Emerging Role in Ovarian Cancer. Int. J. Mol. Sci. 2018, 19, 4122.

Journal reference: Int. J. Mol. Sci. 2018, 19, 4122
DOI: 10.3390/ijms19124122

Abstract

S100A10, which is also known as p11 is located in the plasma membrane and forms a heterotetramer with annexin A2. The heterotetramer, comprising of 2 subunits of annexin A2 and S100A10, activates the plasminogen activation pathway which is involved in cellular repair of normal tissues. Increased expression of annexin A2 and S100A10 in cancer cells leads to increased levels of plasmin which promote degradation of the extracellular matrix, increased angiogenesis and invasion of the surrounding organs. Although many studies have investigated the functional role of annexin A2 in cancer cells including ovarian cancer, S100A10 has been less studied. We recently demonstrated that high stromal annexin A2 and high cytoplasmic S100A10 expression is associated with a 3.4 fold increased risk of progression and 7.9 fold risk of death in ovarian cancer patients. Other studies have linked S100A10 with multidrug resistance in ovarian cancer, however, no functional studies to date have been performed in ovarian cancer cells. This article reviews the current understanding on S100A10 function in cancer with a particular focus on ovarian cancer.

Subject Areas

S100A10; annexin A2; plasmin; ovarian cancer; chemotherapy resistance

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