High brain acid soluble protein 1(BASP1) is a poor prognostic factor for cervical cancer and promotes tumor growth.

Abstract:

BACKGROUND:The aim of this study was to determine whether brain abundant membrane attached signal protein 1 (BASP1) is a valuable prognostic biomarker for cervical cancer and whether BASP1 regulates the progression of cervical cancer. METHODS:Quantitative real-time PCR, western blotting, and immunohistochemistry were used to determined BASP1 levels. Statistical analyses were used to examine whether BASP1 was a prognostic factor for patients with cervical cancer. The MTT assay, colony formation assay, cell cycle assay, anchorage-independent growth assay, and a tumor xenograft model were used to determine the role of BASP1 in the proliferation and tumorigenicity of cervical cancer. RESULTS:Brain abundant membrane attached signal protein 1 was upregulated in cervical cancer tissues and cells, and BASP1 expression levels were higher in patients that had died during follow-up compared with those that survived. There was a positive correlation between BASP1 expression and clinical stage (p < 0.001), T classification (p < 0.001), N classification (p < 0.05), and survival or mortality (p < 0.05). Patients with higher BASP1 expression had a shorter overall survival time. Cox regression analysis shown BSAP1 was an unfavorable prognostic factor for patients with cervical cancer. Overexpression of BASP1 promoted the proliferation of cervical cancer and its colony formation ability, accelerated cell cycle progression, and enhanced tumorgenicity. BASP1 knockdown inhibited the proliferation of cervical cancer and its colony formation ability, suppressed cell cycle progression, and decreased tumorgenicity. CONCLUSIONS:The results showed that BASP1 not only is a novel prognostic factor for patients with cervical cancer, but also promotes the proliferation and tumorigenicity of cervical cancer.

journal_name

Cancer Cell Int

authors

Tang H,Wang Y,Zhang B,Xiong S,Liu L,Chen W,Tan G,Li H

doi

10.1186/s12935-017-0452-4

subject

Has Abstract

pub_date

2017-10-24 00:00:00

pages

97

issn

1475-2867

pii

452

journal_volume

17

pub_type

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