SFXN3 (Sideroflexin 3)

Furthermore, the present study unveils a novel signaling pathway involving REST-SFXN3-Wnt/β-Catenin, which may serve as a therapeutic target. These results provide a valuable insight into the underlying causes of AML and offer a potential framework for precision therapy approaches.

Comparative studies across model organisms reveal both conserved and divergent functions, emphasizing their importance in health and disease. A comprehensive understanding of the SFXN family not only advances fundamental mitochondrial research but also opens avenues for novel therapeutic interventions.

Notably, PFKFB4 was significantly overexpressed in cervical cancer cells and tissue samples, and its silencing markedly inhibited cell migration and invasion. In summary, this study elucidates the molecular mechanisms underlying CC progression and identifies potential candidate biomarkers that could inform treatment strategies for this malignancy.

Further analysis discovered that SFXN5 expression was significantly elevated in neuroendocrinal prostate cancers. In conclusion, SFXN2/4 expressions are novel biomarkers in prostate cancer diagnosis and prognosis.

Increased SFXN3 expression is detected in AML, which indicates a poor prognosis and may link to immunosuppressive state of AML. In addition, SFXN3 can inhibit AML cells apoptosis and promote cell proliferation via enhancing CCND1 and NFKB1 levels.

Conversely, SFXN3 overexpression caused cytosolic iron deficiency with mitochondrial excess Fe(II), which further sensitized HeLa cells to RSL3-induced ferroptosis. In conclusion, we discovered a novel pathway of iron entry into mitochondria from cytosol through PCBP2-TOM20-SFXN3 axis.

In conclusion, SXFN3 plays an important role in the progression and hypermethylation in non-M3 AML patients and could be a potential biomarker for indicating a high CR rate for hypomethylating therapy.

These genes were significantly highly expressed in CRC according to validations in other independent data sets. In conclusion, this study established a network of the co-expressed ceRNAs associated with CRC and identified the genes and miRNAs related to the prognosis of CRC patients.

In vitro experiments found that silencing SFXN3 or TFR2 significantly reduced cell viability. Collectively, our predictive model depended on IMRGs in PTC, which could be potentially utilized to predict the PTC patients' prognosis, schedule follow-up plans, and provide potential targets against PTC.

According to the ENCORI database, four negative regulatory miRNAs for SFXN1 (hsa-miR-22-3p, hsa-miR-140-5p, hsa-miR-532-5p, and hsa-miR-582-3p) and four negative regulatory miRNAs for SFXN2 (hsa-miR-9-5p, hsa-miR-34a-5p, hsa-miR-532-5p, and hsa-miR-885-5p) were related to poor prognosis for BC patients. This study suggests that SFXN1 and SFXN2 are valuable biomarkers and treatment targets for patients with BC.