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World Journal of Pharmaceutical
and Medical Research

An International Peer Reviewed Journal for Pharmaceutical and Medical Research and Technology
An Official Publication of Society for Advance Healthcare Research (Reg. No. : 01/01/01/31674/16)
ISSN 2455-3301
IMPACT FACTOR: 4.103

ICV : 78.6

Abstract

INFLUENCING OF STEROID TO HA-CD44 INTERACTION AND DIVERTS ITS CANCER GROWTH

Fakihi Mohamed*, Prof. L. V. Huixia and Linus Onyinyechi Loveth

ABSTRACT

Catabolism of Hyaluronic acid plays a major pharmacological action since several pathologies were proven. Indeed, induction of pro- angiogenic and inflammatory were enhanced while enzyme imparts different sizes of molecular weight to HA degradation. Research studies emphasized to those enzymes which were played major palliative in reducing the inflammation and damage released onto the extra-matrix cellular that initiate several pathologies. CD44 receptor to HA evoke to play pro- angiogenic and inflammatory actions in breast and ovarian cancer or thyroid associated ophthalmopathy (TAO) and cancer stem cells (CSCs). HA and its binding proteins CD44 regulate the expression of inflammatory genes and beset the intracellular microenvironment phosphate kinase pathway. Thus, interaction HA-CD44 fostered the self-renewal of cancer stem cells (CSCs) and imparts the multidrug resistance due to the ion charge of the HA likewise efflux transporters P-gp. However, steroid compound was found to inhibit Hyaluronic acid action. Furthermore, hyaluronidase was found to facilitate drug absorption by promoting spread. Steroid will suppress HA-CD44 interaction in a fragment minimizing the tumor progression or the multidrug resistance. Indeed, the genetic material was involved in the influence. It is mainly explained with the substitution and traduction of CD variants. Consequently, steroid may contradict the microenvironment pathway by inhibiting the phosphate kinase and enhances the stability of genetic material. Researches should mainly emphasizing the affinity of steroid compound to target the of Hyaluronic acid catabolism and abrogate the stage that involves the labile function of cytoskeleton.

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