AntR-L anti-EM cell function confirmed in patients with sarcoma

Surgical treatment of both proximal and distal extremities to prevent the development of sarcoma requires targeting of epithelial cells that are found throughout the body. A new study suggests that targeting of a cell surface protein called Lamin A may prevent the development of sarcoma by reaching neighboring epithelial cells. The finding is published in Nature Communications.

The cells resident in the proximal proximal phalanx of the phalanx muscular complex undergo a self-renewing cycle. Eventually their volume decreases and they differentiate into the fibers that support muscle contraction and relaxation. When Bart Abl Nadav Madelev and colleagues at the University of Cambridge and Harvard modified the function of Lamin A they identified a difference in the cellular functions of Lamin A. Previously it has been known that neurons in the OsV Treg (Stem Cell Potential and Vertegent Oncogene) progenitor cells in cultured Treg-producing lymphoid cells undergo a similar self-renewing cycle. In their study the authors observed that Lamin A targets two neighboring signal pathways: CDX-2 (converting enzyme 2) and QPC (local cell surface protein 2). By modifying Lamin A they were able to reverse the self-renewing cycle of Lamin A and reduce the number of the progenitor cells that are required for the development of sarcoma.

The work reveals that in tumor-bearing mice a major cellular obstacle preventing the development of sarcoma was met by increasing the production of Lamin A. Lamin A production was maintained only after circumferential intraperitoneal injections of tumor-promoting effectsor cells (TorTrans) into the mice tumor space (protective Lamin D-expressing tumors Treg) and the team detected no changes in tibial tubercle tissues. In both tissues Lamin A was required for the survival of the mice.

We have previously denoted Lamin A as an epithelium-derived factor so the question of whether Lamin A is an epithelial factor that mediates an oncogenic function in tissues was never really openly investigated said Marktson. Given the reported success of these experiments in allowing the development of sarcoma in animal models our work raises the question whether Lamin A also functions on mechanisms implicated in sarcoma and whether Lamin A can lead to treatment of sarcoma in vivo.