Lab study links FAM120A to bladder cancer growth

In bladder cancer cell lines, a protein called FAM120A has emerged as a possible lever for slowing tumor growth and improving the effect of cisplatin, a common chemotherapy drug. The finding comes from researchers at Temple University and partner institutions, who report that suppressing FAM120A appeared to reduce tumor growth and increase cancer-cell sensitivity to the drug.

The protein sits in a signaling chain built around progranulin and EphA2, a receptor previously identified by the researchers as important to tumor establishment and as a potential route for improving chemotherapy. In the new experiments, high FAM120A levels corresponded with stronger progranulin-induced cancer-cell proliferation. Lowering FAM120A produced the opposite pattern, although the exact molecular mechanism remains unclear.

Vrunda Satasiya, Antonio Giordano and Andrea Morrione led the Temple-affiliated work, alongside scientists from Thomas Jefferson University, the University of Milano-Bicocca, the University of Catania and the University of Naples Federico II. Their study, published in the Journal of Experimental & Clinical Cancer Research, describes FAM120A as a novel interactor in this cancer pathway.

And so what, concretely? If later studies confirm the result, FAM120A could offer two practical routes: a target for treatments intended to make bladder cancer more vulnerable to chemotherapy, and a biomarker — a measurable biological sign — that could help characterize the disease or predict its course.

The boundary is clear. These results come from bladder cancer cell lines, not from patients, and the researchers’ proposal to target FAM120A remains a hypothesis.