The Mechanism Of Aptamer C3A Inhibiting The Proliferation Of Breast Cancer Cells

Global cancer statistics show that new cases of breast cancer have surpassed lung cancer.Breast cancer has become the most common cancer and have been seriously threatening women’s health.In clinical treatment,breast cancer is divided into four subtypes,include Luminal A subtype,Luminal B subtype,HER2-enriched expression subtype,and basal-like subtype.The proportion of Luminal A and Luminal B subtype patients is as high as 70%,while the HER2-enriched expression and basal-like subtype account for about 15%,respectively.Current treatments for breast cancer mainly include surgery,radiotherapy and drug therapy.The basal-like subtype has no specific target and cannot be treated with targeted drugs.Although there are many kinds of treatment methods for breast cancer,the treatment effect is still not optimistic.Therefore,we need to develop many therapeutic strategies,to find more general tumor therapeutic targets and develop better tumor-targeted drugs.In recent years,aptamers have been widely researched in tumor diagnosis and treatment,and have the potential to be developed as drugs.This research has found that the C3A affects the viability of breast cancer cells,inhibits proliferation and induce apoptosis.By exploring the mechanism of C3A inhibiting breast cancer cell proliferation,we found that C3A can significantly down-regulate the level of nucleolin.Nucleolin is closely related to cell proliferation and is highly expressed in various cancers including breast cancer.The TCGA database show that nucleolin is highly expressed in breast cancer and is associated with prognosis of patients.The target of C3A is WWP1,and there have no researches showed a direct correlation between C3A and nucleolin.In this study,we explore the mechanism of C3A down-regulating the level of nucleolin.First,we analyze the change in the level of transcription and protein,and find that C3A neither affects the transcription of nucleolin nor promotes the degradation of nucleolin.Second,we clarify that C3A does not down-regulate the level of nucleolin through WWP1.Then,we find that C3A also had no effect on the self-cleavage activity of nucleolin.Finally,we find C3A have altered the solubility of nucleolin,rendering nucleolin become insoluble in RIPA lysate.The paper show that C3A plays a role in inhibiting the growth and proliferation of breast cancer cells by changing the solubility of nucleolin.The research,also find that aptamers can affect the solubility of proteins,which broadens our thought on biological functions of aptamers,and provides a new strategy for the treatment of breast cancer.