Inflammatory signal in aging cells selectively silenced in lab breast cancer cells

When chemotherapy or radiation hits cancer cells, some survive but are no longer healthy. They become senescent cells (also called therapy-induced senescent cells) that release a set of inflammatory molecules. This signalling pattern is known as the senescence-associated secretory phenotype, or SASP. SASP can support cancer recovery but may also stimulate the growth of other tumours.

A microRNA that suppresses SASP

The researchers studied breast cancer cells in the lab and found that a small regulatory molecule called miR-3155b decreases sharply when cells become senescent after chemotherapy (doxorubicin). When they artificially raised miR-3155b levels, concentrations of multiple inflammatory molecules dropped, including IL-6, IL-8, TNF, and MMP13. At the same time, the core features of senescent cells remained intact: the cells still stopped dividing and showed the same DNA damage patterns.

The molecule also worked in a second model (radiation-induced senescence) and in a different breast cancer cell line. It was found to bind directly to the RNA molecules of several SASP factors.

Why this matters for aging

Senescent cells also accumulate during normal aging, independent of cancer. SASP signalling contributes to the chronic low-grade inflammation seen in aging (inflammaging). A molecule that selectively suppresses SASP without destroying the cells is therefore of interest as a research direction beyond oncology. The study was published in Frontiers in Cell and Developmental Biology. The findings have so far only been demonstrated in cultured cells in the lab.

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