Abstract
A majority of small cell lung cancer (SCLC) cells lack a metastasis suppressor, tetraspanin CD9, and CD9 expression promotes their apoptosis. By a proteomics-based approach, we compared an SCLC cell line with its CD9 transfectant and found that a calcium-binding neuronal protein, calretinin, is upregulated in CD9-positive SCLC cells. Ectopic or anticancer drug-induced CD9 expression upregulated calretinin, whereas CD9 knockdown down-regulated calretinin in SCLC cells. When calretinin was knocked down, CD9-positive SCLC cells revealed increased Akt phosphorylation and decreased apoptosis. These results suggest that CD9 positively regulates the expression of calretinin that mediates proapoptotic effect in SCLC cells.
Highlights
Small cell lung cancer (SCLC) is highly malignant lung tumor that spreads early throughout the body
Our previous studies have proposed that the absence of tetraspanin CD9 contributes to highly malignant phenotype of SCLC and that CD9 may be a pivotal regulator of SCLC cell survival [8,9,10]
In the present study using a proteomics-based approach, we identified calretinin as a possible mediator of CD9-induced apoptosis in SCLC
Summary
Small cell lung cancer (SCLC) is highly malignant lung tumor that spreads early throughout the body. It is characterized by neuroendocrine features such as neuropeptide production and N-CAM expression [1]. At diagnosis in most cases, SCLC has already metastasized to regional lymph nodes and distant organs including brain, bone, liver, and adrenal gland, excluding the possibility of surgical resection. Despite its high sensitivity to these anticancer drugs, SCLC rapidly develops recurrent tumors locally and at the distant organs. Such malignant phenotype is at least partially caused by acquired resistance to apoptotic cell death [3].
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