The expression level of CSDAP1 in lung cancer and its clinical significance.

Abstract:

:Expression level of messenger RNA (mRNA) of cold shock domain protein A intronless pseudogene (CSDAP1) in lung cancer tissues was studied. Fresh pathological specimens collected from 317 patients with primary lung cancer through surgical resection from January 2007 to January 2012 were selected. Reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis were used to detect the transcription and translation of CSDAP1 in lung cancer tissues and cancer-adjacent normal tissues, and the results were analyzed in combination with clinicopathological features and prognosis of lung cancer. Among 317 lung cancer specimens, 105 cases (33.1%) had high expression of CSDAP1. Among 138 cases of pulmonary adenocarcinoma, 59 cases had high expression of CSDAP1, and the high expression rate was 42.8%. Among 170 cases of lung squamous cell carcinoma, 46 cases had high expression of CSDAP1, and the high expression rate was 27.5% (P<0.05). Three cases of large cell carcinoma and 9 cases of small cell carcinoma had extremely low expression or had no expression of CSDAP1. Among the 127 lung cancer patients with regional lymph node metastasis, 53 cases (41.7%) had high expression of CSDAP1, while among the 190 lung cancer patients without regional lymph node metastasis, 52 cases (27.4%) had high expression of CSDAP1 (P<0.05). The results also revealed that the expression of CSDAP1 was also related to tumor-node-metastasis (TNM) staging of lung cancer. One-year, three-year and five-year survival rates of lung cancer patients who had no expression of CSDAP1 were relatively high (P<0.05). The results suggested that CSDAP1 may play an important role in the occurrence, development and judgement of prognosis of lung cancer.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Xu T,Li D,He Y,Zhang F,Qiao M,Chen Y

doi

10.3892/ol.2018.9195

subject

Has Abstract

pub_date

2018-10-01 00:00:00

pages

4361-4366

issue

4

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-9195

journal_volume

16

pub_type

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