Figure 1.
Representative images of immunohistochemical staining showing CLPTM1L is overexpressed in lung cancer relative to normal tissues.
(A) Normal lung tissue (×200); (B) Section from lung adenocarcinoma (×200); (C) Section from lung squamous-cell carcinoma (×200); (D) Section from lung adenocarcinoma (×400).
Table 1.
Immunochemistry of human lung tissue.
Table 2.
Clinical parameters.
Figure 2.
Cellular localization of CLPTM1L in 95-D cells.
(A): Western blot analysis for CLPTM1L expression in whole-cell extract, cytosolic and mitochondrial fraction of 95-D cells. (B): 95-D cells were transiently transfected with CLPTM1L-EGFP vector and stained with the mitochondrial marker MitoTracker.
Figure 3.
Overexpression of CLPTM1L in human lung cancer 95-D cells.
(A) The CLPTM1L mRNA level was measured using quantitative real-time PCR in pcDNA3.1(+)-CLPTM1L or pcDNA3.1(+) plasmid transfected cells. *: P<0.05 vs control group (p = 0.001). (B) The expression of CLPTM1L protein was investigated using immunocytochemistry. (C) Effects of CLPTM1L overexpression on cell proliferation in the pcDNA3.1(+)-CLPTM1L transfected cells 95-D cells relative to control 95-D cells. (D) Overexpression of CLPTM1L did not change chemosensitivity to cisplatin in human lung cancer 95-D cells transfected with pcDNA3.1(+)-CLPTM1L relative to controls. The cells were treated with the indicated concentrations of cisplatin for 24 h.
Figure 4.
RNAi-mediated knockdown of CLPTM1L in human lung cancer 95-D cells.
(A) The CLPTM1L mRNA level after RNAi treatment was measured using quantitative real-time PCR in different groups. *: p = 0.000 vs NC control group. (B) The expression of CLPTM1L protein after RNAi treatment was investigated using immunocytochemistry. (C) Growth of shRNA-CLPTM1L transfected cells 95-D cells and control 95-D cells for 72 h. (D) shRNA-CLPTM1L transfected cells 95-D cells and control 95-D cells were treated with indicated concentration of cisplatin for 24 h. *: p = 0.003 vs NC control group (25 µM) and #: p = 0.006 vs NC control group (50 µM).
Figure 5.
Knockdown of CLPTM1L increased cisplatin-induced activation of caspase-3/7 and caspase-9.
shRNA-CLPTM1L transfected 95-D cells and control cells were treated with 50 uM cisplatin for 24 h. Caspase-3/7 and caspase-9 activity were measured and the results were represented as fold increase of the activity of the cells without cisplatin treatment. *: p = 0.004 vs NC control group (caspase-3/7) and #: p = 0.000 vs NC control group (caspase-9).