Affiliations: [a] Central Lab, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China | [b] Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
Correspondence:
[*]
Corresponding authors: Xuming Luo, Department of Respiratory Medicine, Putuo Hospital, Shanghai
University of Traditional Chinese Medicine, Shanghai, China. E-mail:
[email protected]; Xiongbiao Wang, Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. E-mail:
[email protected]
Abstract: BACKGROUND: CLPTM1L (Cleft lip and palate transmembrane protein 1-like) has
been previously shown to be overexpressed in lung cancer and is involved in
regulating cisplatin sensitivity. In this study, we assessed the
relationship between CLPTM1L expression and prognosis of lung cancer in
patients and explored its role in regulating cell migration and invasion. METHODS: Immunohistochemistry was used to examine CLPTM1L expression levels
on a tissue microarray containing 73 sets of human lung cancer specimens
with adjacent normal tissue. The correlation between CLPTM1L expression and
patient survival was analysed by the Kaplan-Meier method. In addition,
CLPTM1L-knockdown lung cells were used to investigate the effect of CLPTM1L
on cell migration and invasion in vitro. RESULTS: The results of immunohistochemical
analysis showed that CLPTM1L was overexpressed in lung cancer tissues
compared with adjacent normal tissues. Kaplan-Meier analyses revealed that
patients with high CLPTM1L expression showed poorer survival than those with
low CLPTM1L expression. In addition, in vitro studies revealed that the knockdown of
CLPTM1L expression in 95-D lung cancer cells suppressed cell migration and
invasion. Further, the loss of CLPTM1L resulted in decreased matrix
metalloproteinase-2 (MMP-2) expression in these cells. CONCLUSION: Our data demonstrate that CLPTM1L overexpression can predict poor prognosis in
patients with lung cancer and suggest that CLPTM1L might be associated with
the regulation of cell migration and invasion.
