Establishment of cohesion 1 homolog 2 facilitates cell aggressive behaviors and induces poor prognosis in renal cell carcinoma.

Qiu‐Li Wang,Ling Liu

doi:10.1002/jcla.23163

Abstract

Background and aimsEstablishment of cohesion 1 homolog 2 (ESCO2) has been identified as an essential factor for cohesion in cell cycle in human multiple cancers. Nonetheless, its functional implication on prognosis and cellular behaviors of renal cell carcinoma (RCC) is rarely elucidated. We performed this study to detect the effects of ESCO2 in RCC progression.MethodsWe accessed The Cancer Genome Atlas (TCGA) database to evaluate the ESCO2 expression levels in tumor tissues, including 32 normal tissues and 289 tumor tissues. Quantitative real‐time PCR and Western blot were implemented for expression detection. After ESCO2 knockdown using siRNAs interference, functional experiments were conducted to explore the role of ESCO2, such as cell proliferation analysis and colony formation assay. Transwell assays for migration and invasion was also performed.ResultsIn this study, ESCO2 was significantly increased in RCC tissues and cell lines. The RCC patients with high expression of ESCO2 were susceptible to unfavorable prognosis, and its expression has a marked association with clinical features containing age, gender, pathologic stage, and so on. Furthermore, knockdown of ESCO2 inhibited cell growth, invasion, and migration. Mechanistically, phosphorylation protein kinase B (AKT) and mammalian target of rapamycin (mTOR), proliferating cell nuclear antigen (PCNA), and p53 were all down‐regulated due to the ESCO2 inhibition.ConclusionsTherefore, our results raised the possibility that ESCO2 may act as a promising option for tumor therapeutic interference by exhibiting enhanced selectivity over conventional chemotherapy.

Highlights

Kidney cancer ranks second in urogenital tumors in the world with an increasing incidence and mortality rate of 2.2% and 1.8% in 2018, respectively.[1]
The results showed that Establishment of cohesion homolog 2 (ESCO2) was excluded successfully by qRT-PCR method and Western blot analysis (Figure 2A-C, P < .01)
After knockdown ESCO2, we found that the expressions of p-AKT and p-mammalian target of rapamycin (mTOR) were significantly decreased

Summary

| INTRODUCTION

Kidney cancer ranks second in urogenital tumors in the world with an increasing incidence and mortality rate of 2.2% and 1.8% in 2018, respectively.[1]. The response to the mentioned treatments is un-effective.[3] we hope that the great progress in targeted treatments would emerge with the fully understanding of RCC pathogenesis in the future. Fumiichiro and Miyako examined the genes change, found that up-regulation of ESCO2 was striking in breast cancer tissues and cell lines.[9] Notably, the dysregulated ESCO2 was implicated to adjust metastatic activity in colorectal cancer (CRC), suppressing Matrix Metallopeptidase 2 (MMP2).[10] Yet, whether and how the progression of RCC is controlled by ESCO2 has not been resolved. We performed this study to assess the expression of ESCO2 in RCC tissues and cell lines, investigated the association between ESCO2 and prognosis of patients with RCC and detected the biological role of ESCO2 knockdown on the cellular malignant behaviors in vitro. The potential mechanism underlying the impact of ESCO2 in RCC progression was explored using Western blot analysis

| MATERIALS AND METHODS

Findings

| DISCUSSION

| CONCLUSIONS