FTO expression

FTO plays a significant role in CRC progression by regulating PKM2 and promoting glycolysis.

The presented data collectively suggest that chronic cadmium treatment may impact the m6A level through influencing regulatory proteins, which could potentially trigger oxidative stress and apoptosis by regulating transcription factors such as NF-κB and NRF2. In conclusion, our study provides a scientific foundation for understanding cadmium toxicity and offers novel insights for treating cadmium-induced lung diseases.

Our study unveiled CCL15 as a key mediator in HCC progression, facilitating communication between HCC cells and CAFs. This highlights a novel regulatory axis in HCC and suggests that targeting CCL15 could be a potential therapeutic strategy.

This study reveals that HIF-1α promotes FTO transcription under hypoxic conditions, thereby increasing PD-L1 expression through the PDK1/AKT/STAT3 axis. Inhibition of FTO and PDK1 under hypoxic conditions could serve as a promising immunotherapeutic strategy for breast cancer.

All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer.

The fact that WTAP protein expression levels lower while WTAP RNA expression remains high, lets us hypothesize a sort of inhibition of protein expression, but further studies are needed to clarify the mechanism. Although the results suggest a relationship between biological meaning and prognostic utility of WTAP, this prognostic utility must be confirmed by further studies on a larger sample.

Our study proposes that hsa_circ_0112136 functions as a tumor promoter, facilitating the malignant progression of GC through m6A modification (suppressed by FTO) and activating the PI3K/AKT/mTOR pathway. This suggests that targeting FTO-m6A-hsa_circ_0112136-PI3K/AKT/mTOR may be a novel approach for GC intervention.

Our research elucidated the functional importance of FTO-mediated m6A demethylation of MTUS1/ATIP1, suggesting that targeting the FTO-MTUS1/ATIP1 axis could be a prospective novel approach for treating HNSCC.

Finally, we demonstrated that the NF-κB inhibitor Bortezomib further enhances DNMT2 deletion-induced apoptosis in hepatocellular carcinoma cells. This study reveals DNMT2's role in liver cancer and presents a new therapeutic target for future treatments.

HKL induced autophagy and inhibited cell migration in MG63 cells by increasing the expression of FTP and Smad6. It can be seen that HKL may be a promising drug for the treatment of OS.

We identified elevated levels of FTO in OS, which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes. It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.

In conclusion, FOXF2 alleviates ESCC via promoting the transcription of RNF144A which results in the ubiquitylation and degradation of FTO. Targeting FOXF2/RNF144A/FOT axis might be a possible strategy for the treatment of ESCC.