Context:
Researchers at Delhi’s CSIR-Institute of Genomics and Integrative Biology (IGIB) have for the first time identified a calcium sensor protein (STIM1) that independently regulates both skin cancer and pigmentation. The STIM1 protein does so by activating two independent signalling pathways.
Parts of the STIM1:
- Interestingly, different parts of the STIM1 protein activate the two independent signalling pathways that control melanoma growth and pigmentation.
- This opens up the possibility of developing drug molecules that target specific sites in the STIM1 protein to control tumour growth and regulate pigmentation.
- While skin cancers account for third highest number of cancer associated deaths worldwide, perturbations in pigmentation pathways result in pigmentation disorders such as solar lentigo, melasma, vitiligo, and pityriasis alba. Current therapeutic regimes are not efficient in alleviating pigmentation disorders.
Role of STIM1
- The role of STIM1 in breast cancer and prostrate cancer is already known.
- STIM1 might have a role in melanoma growth as well.
- To study the role of STIM1 protein in melanoma growth in vitro, the researchers used STIM1 knockdown mouse cells and injected them into mouse models and observed the growth of melanoma. Compared with controls, melanoma growth was reduced by as much as 75% in mice that were injected with STIM1 knockdown cells.
- STIM1 protein, which is a key regulator of calcium signalling pathway, would be regulating pigmentation too.
Zebrafish embryos:
- To confirm the role of STIM1 protein in pigmentation, the researchers knocked down the protein in melanocytes. This resulted in a reduction in pigmentation levels. “We further validated the role of STIM1 in regulating pigmentation in zebrafish models.
- The knockdown of STIM1 significantly decreased pigmentation in zebrafish embryos. Both in vitro and zebrafish studies established the critical role of STIM1 protein in pigmentation.
- The protein mediates calcium entry into cells and this leads to melanoma growth.
Source:TH