富含亮氨酸的小蛋白多糖(SLRP)家族在细胞外基质中广泛表达并加重肿瘤进展。然而,phycan(EPYC),作为SLRP家族的一员,其在癌症中的生物学功能尚未得到证实。因此,我们旨在阐明EPYC在卵巢癌(OC)进展中的作用,并进一步分析了与肿瘤发生有关的分子机制。这里,我们分析了GSE38734的差异表达基因,包括4个匹配的原发性OC和转移组织。我们从癌症基因组图谱(TCGA)中获得了OCRNAseqs数据,并分析了EPYC表达与OC分期的相关性。病理分级,等。在Oncomine网站上比较了卵巢癌和正常卵巢组织中EPYC的表达。我们使用siRNA干扰卵巢癌细胞系SKOV3中EPYC的表达。划痕试验,Transwell-Matrigel室,CCK8法检测SKOV3迁移的变化,EPYC被干扰后的侵袭和增殖能力。我们用R软件对EPYC的相干基因做GO和KEGG剖析。我们使用Hitprediction网站来预测相互作用的蛋白质。成果显示EPYC在转移性卵巢癌中的表达高于原发性卵巢癌,原发癌高于正常卵巢。siRNA干扰EPYC表达后,移民,SKOV3细胞的侵袭和增殖削弱。EPYC主要在ECM组织中发挥作用,参与PI3K/Akt,粘着斑信号通路。EPYC可能与PLCG2和CRK相互作用,并参与信号转导。
The small leucine-rich proteoglycan (SLRP) family is widely expressed in extracellular matrix and aggravates tumor progression. However,
epiphycan (EPYC), as a member of the SLRPs family, its biological function in cancer has not been confirmed. Thus, we aimed to clarify the role of EPYC in progression of ovarian cancer (OC), and further analyze the molecular mechanisms implicated in tumorigenesis. Here, we analyzed the differential expression genes of GSE38734, including 4 matched primary OC and metastatic tissues. We obtained OC RNAseqs data from the Cancer Genome Atlas (TCGA) and analyzed the correlation between EPYC expression and OC staging, pathological grading, etc. The expression of EPYC in OC and normal ovarian tissues was compared in Oncomine website. We used siRNAs to interfere the expression of EPYC in ovarian cancer cell line SKOV3. Scratch test, transwell-matrigel chamber, CCK8 assay were used to detect the changes of SKOV3 migration, invasion and proliferation ability after EPYC was interfered. We used R software to make GO and KEGG analysis of related genes of EPYC. We used the Hitpredict website to predict interacting proteins. The results showed that the expression of EPYC in metastatic ovarian cancer was higher than primary ovarian cancer, and that in primary cancer was higher than normal ovaries. After siRNA interferes with EPYC expression, the migration, invasion and proliferation of SKOV3 cells were weakened. EPYC mainly played a role in ECM organization, and involved in PI3K/Akt, focal adhesion signaling pathways. EPYC might interact with PLCG2 and CRK, and be involved in signal transduction.