Genetic Variation in PDCD6 and Susceptibility to Lung Cancer

Abstract

Lung cancer is the most common type of cancer and one of the leading causes of death in the world. Genetic factors play an important role in its development. PDCD6, the encoding gene for programmed cell death protein 6, may function as a tumor suppressor gene. Non-small cell lung cancer (NSCLC) contributes about 80% to newly histologically diagnosed lung cancer patients. To explore the relationship between PDCD6 and NSCLC, we examined two single nucleotide polymorphisms(rs3756712 G/T andrs4957014 G/T, both in the intron region) of the PDCD6gene.A hospital-based case-control study was carried out including 302 unrelated NSCLC patients and 306 healthy unrelated subjects. Significantly increased NSCLC risk was found to be associated with the T allele of rs4957014 (P=0.027, OR=0.760, 95%CI=0.596-0.970). The genotype and allele frequencies of rs3756712 did not shown any significant difference between NSCLC group and controls (P=0.327, OR=0.879, 95%CI=0.679-1.137). In conclusion, we firstly demonstrated the association between the PDCD6 gene and risk of NSCLC in a Chinese Han population.

Systematic identification of lincRNA‐based prognostic biomarkers by integrating lincRNA expression and copy number variation in lung adenocarcinoma

“…59,60 One single nucleotide polymorphism rs4957014 in the intron region of the PDCD6 gene significantly increased NSCLC risk. 61 SiRNA-mediated knockdown of CKS1B resulted in a significant decrease in lung cancer cell proliferation, invasion, and migration and sensitized the response of lung cancer cell lines to cisplatin and paclitaxel. Cyclin-dependent kinase CKS1B regulates lung cancer progression and chemoresistance.…”

“…Studies of lung cancer demonstrated that PDCD6 overexpression was indicative of poor prognosis for patients with early stage NSCLC or LUAD . One single nucleotide polymorphism rs4957014 in the intron region of the PDCD6 gene significantly increased NSCLC risk . SiRNA‐mediated knockdown of CKS1B resulted in a significant decrease in lung cancer cell proliferation, invasion, and migration and sensitized the response of lung cancer cell lines to cisplatin and paclitaxel.…”

Association of PDCD6 polymorphisms with the risk of cancer: Evidence from a meta-analysis

“…Four studies [ 42 , 45 , 44 , 9 ] reported the association between rs3756712 and rs4957014 polymorphisms and cancer. As shown in Figure 3 and Table 2 , the results showed that PDCD6 rs3756712 T>G polymorphism was significantly associated with decreased risk of cancer under codominant (OR = 0.82, 95%CI = 0.70–0.96, p = 0.01, TG vs TT; OR = 0.53, 95%CI = 0.39–0.72, p < 0.0001, GG vs TT), dominant (OR = 0.76, 95%CI = 0.66–0.89, p = 0.0004, TG+GG vs TT), recessive (OR = 0.57, 95%CI = 0.43–0.78, p = 0.0003, GG vs TT+TG), and allele (OR = 0.76, 95%CI = 0.67–0.86, p <0.00001, G vs T) genetic model.…”

“…Previous studies inspecting the association between PDCD6 gene polymorphisms and cancer indicated inconclusive and contradictory results [ 9 , 45 , 44 , 42 ]. Hence, we have performed a meta-analysis on all the published case-control studies to evaluate the association of PDCD6 rs3756712 T>G and rs4957014 T>G gene polymorphisms with the risk of cancer.…”

Whole exome sequencing identifies novel candidate mutations in a Chinese family with left ventricular noncompaction

“…PDCD6 is a calcium-binding modulator associated with cell proliferation and death (38). Numerous studies have revealed that PDCD6 is associated with tumors; however, the underlying mechanism remains unclear (39)(40)(41)(42). Furthermore, one study demonstrated that overexpression of PDCD6 suppressed angiogenesis in vitro via the phosphatidylinositol 3-kinase/protein kinase mTOR/ribosomal protein S6 kinase B1 pathway (43).…”