TFAM (Transcription Factor A, Mitochondrial)

We have provided fresh insights into the crosstalk between telomere and mitochondrial biology in CRC precursors. These findings hold promise in understanding adenoma formation and CRC progression, as mtDNA-CN elevation and its association with TL were specific to precancerous lesions and were lost with progression to tumor.

These studies reveal that BMPR2 signaling regulates TAK1-d splice variant to mediate mitochondrial Ca2+ transport, which is dependent on the MCU. Our studies suggest that BMPR2 signaling utilizes mtCa2+ transport to regulate both mitochondrial bioenergetics and/or cell survival. Our studies provide novel insight into how aberrant BMPR2 signaling is pathogenic and suggests that the response could vary depending on the cell type.

Mechanistically, ETV6 binds to the miR-429 promoter, mediating glucose metabolic reprogramming in HCC cells by targeting CRKL via the PI3K/AKT pathway. Taken together, these findings reveal that the ETV6-miR-429-CRKL regulatory circuitry plays a crucial role in glucose metabolic reprogramming in HCC, offering novel insight and a potential target for cancer therapy.

Treatment with sEV-miR-206-3p effectively mitigated these alterations, reducing oxidative stress, suppressing neuroinflammatory responses, restoring mitochondrial function and synaptic protein levels, and attenuating tau and Aβ pathology. These findings demonstrate that miR-206-3p-loaded sEVs protect neuroblastoma cells from Aβ-induced neurodegenerative processes, highlighting their potential as a novel drug delivery system for neuroprotection.

We further show silent mating type information regulation2 homolog-3 (SIRT3)-mediated deacetylation stabilizes TFAM, whereas SIRT3 downregulation promotes TFAM degradation via polyubiquitination. Together, our study reveals a novel mode of metabolic reprogramming due to the loss of TFAM and identifies the TFAM-G6PD axis as a metabolic vulnerability, offering a promising synthetic lethal therapeutic strategy for liver cancer.

PTMA preserved mitochondrial DNA integrity through interaction with mitochondrial transcription factor A (TFAM), sustaining T cell oxidative phosphorylation under metabolic stress. Our findings identify the TCF1-PTMA axis as a molecular link between mitochondrial fitness and durable T cell-mediated antitumor immunity, offering insights and potential directions for future therapeutic strategies to boost immunotherapy efficacy.

Molecular docking studies suggested that phloroglucinol may exert its effects via interaction with the Kelch-like ECH-associated protein 1 (KEAP1)-Nrf-2 pathway. These findings highlight phloroglucinol as a promising multi-target neuro-protective agent for ischemic stroke, warranting further investigation for clinical translation.

These findings reveal that FGF9 enhances mitochondrial biogenesis in glioblastoma through the CREB-PGC-1α-TFAM axis, uncovering a novel metabolic mechanism underlying its pro-tumorigenic effects.

Molecular docking highlighted Monomethyl lithospermate as a key active component. Overall, SLC influences oxidative phosphorylation via the PDK1/PDHA1 and SIRT1/PGC-1α/NRF1/TFAM signaling pathways and downregulates the HER2 pathway, thereby ultimately inhibiting HER2-positive breast cancer progression.

OXPHOS augmentation (by α-ketoglutarate [αKG]) or suppression (by metformin) disrupt Treg metabolism. Finally, indoleamine 2,3-dioxygenase (IDO) seems to affect Tregs and can be a promising target in advanced immunotherapy naïve cancer patients. The focus of this review is to describe Treg metabolic regulators/connectome and opportunities they bring about in cancer therapy.

Immunohistochemistry and genetic analysis are important tools to differentiate MASC from its morphological mimickers. The treatment approach for MASC has not been well defined or standardised, necessitating further studies to develop evidence-based guidelines.