LPCAT3 (Lysophosphatidylcholine Acyltransferase 3)

Harmine exerts antitumor effects in NSCLC by inducing ferroptosis through direct targeting of PDE4D and suppression of the PI3K-Akt-Nrf2 pathway, highlighting PDE4D as a novel therapeutic target and harmine as a promising candidate for NSCLC treatment.

AA induces ferroptosis in HCC through the SIRT5-ACSL4/LPCAT3/ALOX15 pathway, offering mechanistic insight into lipid metabolism-related ferroptotic regulation.

Treatment with the GPX4 inhibitor RSL3 enhanced the anti-persister effects of endocrine-based therapies in xenograft-bearing mice. These findings supporting the development of therapeutic strategies to leverage the oxidative stress induced by endocrine-based therapies and drive ferroptosis as a treatment for ER+ breast cancer. Endocrine therapy increases oxidative stress and sensitizes endocrine-tolerant persister ER+ breast cancer cells to ferroptosis, indicating that therapies targeting this metabolic dependency could help prevent disease recurrence and progression.

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.

LPCAT3was identified as a ccRCC biomarker and may regulate immune infiltration and prognosis in ccRCC by mediating ferroptosis and ERS. Thus, it has potential for exploitation as a prognostic and immune therapeutic target for patients with ccRCC.

LPCAT3 modulated metabolism of arachidonic acid, thereby regulating ferroptosis and the survival signaling to determine cancer growth and metastasis.

Moxibustion at BL23 and ST36 can alleviate synovial inflammatory injury, and its mechanism may be related to reducing lipid peroxidation and ROS levels, and inhibiting the occurrence of ferroptosis.

SPXJF exerts anti-tumor effects on HCC cells by inducing ferroptosis, and its mechanism of action involves the regulation of ferroptosis-related genes and proteins. This study provides a theoretical basis for the clinical treatment of HCC and the development of new anti-cancer drugs, offering a valuable contribution to the field of ethnopharmacology.

Our study suggests that apoptosis and ferroptosis act together in VA-mediated tumor suppression in MCF-7 breast cancer cells. These findings suggest that VA, an anti-neoplastic agent, could potentially treat luminal A targeted breast cancer via the ferroptosis pathway.

Our study identified the cell m6A methylation change lists after repeated UVB irradiation, and revealed that FTO and LPCAT3 play key roles in the m6A methylation pathogenesis of UV-induced skin cell apoptosis. FTO-m6A-LPCAT3 might serve as a novel upstream target for preventing and treating photoaging and UV-induced skin diseases.

Overall, our data reveal a previously unrecognized role of the MALT1-LPCAT3 axis in osteoarthritis. Targeting the MALT1-LPCAT3 pathway with MALT1 inhibitors or siRNA-liposomes of LPCAT3 may become an effective strategy to treat OA by suppressing eicosanoids, matrix-degrading enzymes, and proinflammatory cytokines.

In conclusion, our study demonstrated a novel mechanism by which LPCAT3 is regulated, and demonstrated that Mef is a highly promising new target that can be utilized to enhance the efficacy of anti-PD-1 immunotherapy.