title: A Preliminary Study on RCN3 Protein Expression in Non-small Cell Lung Cancer.
abstract: BACKGROUND
  Reticulocalbin 3 (RCN3), a member of CREC (Cab45/reticulocalbin/ ERC-45/calumenin) family protein, is located in the secretory pathway of endoplasmic reticulum (ER) of living cells. Disruption of RCN3 leads to failure of lung function in the mouse model. Although ER stress has been associated with the development of a variety of tumors, the role of RCN3 in development of non-small cell lung cancer (NSCLC) in human is unknown at present.
  
  
  METHODS
  In this study a total of 41 paired NSCLC specimens (cancer group) and the adjacent normal tissues (control group) were obtained from patients undergoing lung lobectomy or pneumonectomy surgeries in Beijing Shijitan Hospital, Capital Medical University. The RCN3 mRNA and protein level in each clinical sample was determined using quantitative real time-PCR and immunoblotting, respectively. Immunohistochemistry analysis was utilized to compare the protein expressional patterns of RCN3 between the two clinical sample groups.
  
  
  RESULTS
  Immunoblotting showed that levels of RCN3 protein in the NSCLC tissues were significantly lower than those in the control group (p < 0.001), suggesting ER stress is closely associated with the cancer cells. Accordingly, the ER stress protein GRP78 (glucose-regulated protein 78, also known as BIP) was remarkably upregulated in the cancer group (p < 0.05). Within the cancer group, a significant difference in RCN3 protein expression was observed in squamous cell carcinoma versus adenocarcinoma (p < 0.05). In the lung cancer group, however, RCN3 protein levels were not correlated with the age and the gender. In addition, RCN3 mRNA levels showed no significant difference between the cancer and the control groups, suggesting that the differential regulation of RCN3 is likely at post-transcription stage in NSCLC.
  
  
  CONCLUSIONS
  Our study showed that RCN3 protein level was significantly down regulated in NSCLC, suggesting a potential correlation between RCN3 protein depletion and development of NSCLC. Although the exact cause-effect relationship between RCN3 and NSCLC needs to be further investigated, the study helps to shed additional lights on the molecular regulation of the lung cancer.
authors.forename: Yu
authors.initials: Y
authors.lastname: Hou
authors.forename: Yongchao
authors.initials: Y
authors.lastname: Li
authors.forename: Fuxing
authors.initials: F
authors.lastname: Gong
authors.forename: Jiawei
authors.initials: J
authors.lastname: Jin
authors.forename: Aiben
authors.initials: A
authors.lastname: Huang
authors.forename: Qiuhong
authors.initials: Q
authors.lastname: Fang
authors.forename: Runlin Z
authors.initials: RZ
authors.lastname: Ma
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002135:Calcium-Binding Proteins / Q000032:analysis* / Q000235:genetics; D002289:Carcinoma, Non-Small-Cell Lung / Q000737:chemistry*; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000737:chemistry*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D002135:Calcium-Binding Proteins; D000091342:Endoplasmic Reticulum Chaperone BiP; C000717247:HSPA5 protein, human; C000717248:Hspa5 protein, mouse; C510564:RCN3 protein, human; D012333:RNA, Messenger