MIR532 (MicroRNA 532)

RNase R digestion and actinomycin D assays were employed to assess its stability...Animal experiments confirmed that silencing circ_0017521 suppressed tumor growth and glycolysis. This study revealed that hypoxia-induced circ_0017521 activated the PI3K/AKT pathway through the miR-532-3p/PFKFB3 axis, synergistically driving EMT and glycolysis, thereby promoting NSCLC progression.

These findings highlight the transformative potential of exosomal ncRNAs in precision oncology, offering novel ways for non-invasive diagnostics, prognostic stratification, and targeted therapies in hematological malignancies. Additional studies are necessary to validate these biomarkers and explore their clinical applications.

Priorities for validation include reporter assays, gene/protein modulation, phenotypic rescue, and in vivo testing in MP-exposed models. Collectively, our results nominate miRNAs as candidate tools to interrogate and potentially mitigate MP-associated carcinogenic mechanisms.

Preclinical studies demonstrate that MEL enhances chemoradiotherapy efficacy-reducing tumor volume by 70% in murine colorectal models and decreasing 5-fluorouracil (5-FU) resistance via miR-532-3p/β-catenin axis modulation...Given its low toxicity and putative synergy with immunotherapies, MEL should be regarded as an adjunct under investigation rather than an established option; to date, no GI-specific phase III randomized trials exist, and clinical signals come primarily from small, heterogeneous cohorts. Dosing is unstandardized and limited by low oral bioavailability (first-pass) and possible pharmacogenomic variability.

Meanwhile, exosomal transfer of VPS9D1-AS1 sequestered miR-532-3p to up-regulate catenin beta 1 (CTNNB1). Taken together, exosomal transfer of VPS9D1-AS1 induced M2 polarization to promote erlotinib resistance of LUAD cells through activating Wnt/β-catenin pathway.

Mechanistic and functional studies in both in vivo and in vitro settings revealed that highly expressed circRAB23 acts as a sponge for miR-532-3p, deregulating the inhibitory effect of miR-532-3p on HMGA2 and thereby affecting the epithelial mesenchymal transition (EMT)-related signalling pathway and promoting tumour cell invasion and metastasis. In conclusion, circRAB23 promotes malignant proliferation and metastasis in ICC via the miR-532-3p/HMGA2/EMT axis, making it a promising diagnostic and therapeutic target for ICC.

Author Y. Zhang did not indicate their agreement with the retraction. Authors T. Luo, H. Guan, J. Liu and J. Wang did not respond to communications from the Publisher regarding the retraction.

The two key regulatory axes, hsa_circ_0072088/hsa-miR-532-3p/MMP14 and hsa_circ_0049271/hsa-miR-224-5p/DCN, might be involved in carcinogenesis, prognosis and immune infiltration of LUAD.

LPCAT3 overexpression antagonized the effects of miR-532-3p overexpression on the proliferation, apoptosis, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells. These findings suggested that CircCOG5 could modulate the ferroptosis of OVCAR-3 and SKOV3 cells through targeting regulation of miR-532-3p/LPCAT3.

Downregulation of miR-532-3p or overexpression of AMOTL2 abolished the effect of silencing circ_0001461. Collectively, our research demonstrated that the circ_0001461 played a certain regulatory role in growth, movement and immune escape of colon cancer via miR-532-3p/AMOTL2 axis.

Overexpression of hsa_circ_0087104 suppressed in vitro migration and invasion of ESCC cells and this suppressive effect could be weakened by upregulation of miR-542-3p. Collectively, the current findings elucidated a potential hsa_circ_0087104/miR-542-3p/PIK3R1 axis that might be involved in suppression of lymph node metastasis of ESCC.