Bladder cancer (BCa), one of the most common and deadly malignancies of the urinary system, is characterised by high rates of recurrence and rapid progression.

Exosomes and long non-coding RNAs (lncRNAs) are key players in tumour development, with lncRNAs comprising 3.36% of the total RNA content in exosomes.

Although exosomal lncRNAs are essential regulators of BCa, their underlying mechanisms remain poorly understood.

This research published in the Genes & Diseases journal by a team from Wuhan University evaluated the role of exosomal lnc-TAF12–2:1 in the promotion of BCa.

The research team performed lncRNA chip sequencing of urinary exosome RNA collected from BCa patients and identified lnc-TAF12–2:1 as highly expressed in these patients.

Functional assays revealed that silencing of lnc-TAF12–2:1 inhibited tumour growth, enhanced cell cycle arrest, and induced apoptosis, while its overexpression had the opposite effect—both in vitro and in xenograft mouse models.

Interestingly, the researchers found that exosomal lnc-TAF12–2:1 exerted its function through exosomal intercellular transmission.

Further analysis showed lnc-TAF12–2:1 to be predominantly localised in the cytoplasm and tends to form a competing endogenous RNA (ceRNA) regulatory network.

A dual luciferase reporter assay, RIP, and RNA pulldown assays confirmed the interaction of lnc-TAF12–2:1, miR-7847–3p, and ASB12.

Similar to lnc-TAF12–2:1, down-regulation of ASB12 expression repressed BCa cell proliferation and migration, while promoting cell cycle arrest at the G0/G1 phase and inducing apoptosis.

Mechanistically, exosomal lnc-TAF12–2:1 acted as a sponge for miR-7847–3p, alleviating miRNA-mediated silencing of ASB12 and thereby promoting BCa progression.

Importantly, this study also confirmed that ASB12 functions as an oncogene, promoting cell proliferation and migration while inhibiting cell cycle arrest and apoptosis.

In conclusion, this study suggests that exosomal lnc-TAF12–2:1 is a novel diagnostic and therapeutic biomarker that functions by influencing the miR-7847–3p/ASB12 regulatory axis in BCa.

Source: Compuscript Ltd