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Gajendran, N.

Publications and source records attributed to Gajendran, N..

2 recordsLinked to original sources

Transcriptomic analysis of melanoma cells reveals an association of α-synuclein with regulation of the inflammatory response.

The Parkinsons disease protein, alpha-synuclein (-syn/SNCA), is highly expressed in neurons and melanomas. The goal of this study was to reveal the mechanism(s) of -syns involvement in melanoma pathogenesis. To decipher the genes and pathways affected by -syn, we conducted an RNA sequencing analysis of human SK-MEL-28 cells and several SK-MEL-28 SNCA-KO clones. We identified 1098 significantly up-regulated genes and 660 significantly down-regulated genes. Several of the upregulated genes are related to the immune system, i.e., the inflammatory response and the matrisome. We validated five upregulated genes (IL-1y, SAA1, IGFBP5, CXCL8, and CXCL10) by RT-qPCR and detected IGFBP5 and IL-1y in spent media of control and SNCA-KO cells. The levels of each of these secreted proteins were significantly higher in the spent media of the SNCA-KO clones than control cells. We suggest that the loss of -syn expression unleashes chemokine/cytokine secretion, which could help melanoma cells evade the immune system.

cancer biology↗

Knocking out alpha-synuclein in melanoma cells downregulates L1CAM and decreases motility

The Parkinsons disease (PD) associated protein, alpha-synuclein (-syn/SNCA), is highly expressed in aggressive melanomas, which raises the possibility that -syn has a pro-survival function in melanoma. Herein, we asked whether -syn modulates the expression of the pro-oncogenic adhesion molecules L1CAM and N-cadherin. We used two human melanoma cell lines (SK-MEL-28, SK-MEL-29), SNCA-knockout (KO) clones, and two human SH-SY5Y neuroblastoma cell lines. In the melanoma lines, loss of -syn expression resulted in significant decreases in the expression of L1CAM and N-cadherin and concomitant significant decreases in motility. On average, there was a 75% reduction in motility in the four SNCA-KOs tested compared to control cells. Strikingly, comparing neuroblastoma SH-SY5Y cells that have no detectable -syn to SH-SY5Y cells that stably express -syn (SH/+S), we found that expressing -syn increased L1CAM and single-cell motility by 54% and 597%, respectively. The reduction in L1CAM level in SNCA-KO clones was not due to a transcriptional effect, rather we found that L1CAM is more efficiently degraded in the lysosome in SNCA-KO clones than in control cells. We propose that -syn is pro-survival to melanoma (and possibly neuroblastoma) because it promotes the intracellular trafficking of L1CAM.

cancer biology↗