PLAGL2 (PLAG1 Like Zinc Finger 2)

This study indicated that SAPCD2 could serve as a critical driver of BCa malignancy, emphasizing its role in sustaining oncogenic signaling through the SAPCD2-TANK-MAPK axis and the PLAGL2-SAPCD2-CREB feedback loop. Targeting this pathway may offer novel therapeutic strategies for treating aggressive BCa.

They also represent the first PLAG1 fusions identified in pediatric supratentorial ependymal tumors. These cases highlight the value of integrating histology, methylation profiling, and fusion detection, and suggest a new candidate supratentorial ependymal subtype with PLAG1 fusions, pending validation in larger series.

It effectively inhibited tumor growth in HCCLM3 xenograft tumor models while demonstrating a favorable safety profile. Taken together, this study introduces a promising 3-(Phenylsulfonamido) benzamide derivative as a novel approach to targeting PLAGL2 transcriptional activity, laying a foundation for future investigations in anti-tumor therapy.

Therefore, the article must be retracted. The authors did not respond to communications from the Publisher regarding the retraction.

Following this manipulation, the cells are subjected to treatment with or without doxycycline...Subsequently, luciferase reporters and chromatin immunoprecipitation (ChIP)-PCR assays reveal that MFSD12 is regulated positively by pleomorphic adenoma gene like-2 (PLAGL2), an important transcription factor. Collectively, our results indicate that MFSD12 exerts a tumor-promoting effect on BLCA progression, under the modulation of transcription factor PLAGL2.

In summary, we describe a third subtype of PLAG family-altered pediatric CNS embryonal tumor characterized by PLAG1 gene fusion, which leads to upregulation of PLAG1 and downstream genes. We therefore propose to rename ET, PLAGL to ET, PLAG (CNS embryonal tumor with PLAG family gene alteration) together with a specification of the respective subtype.

This study demonstrated that the expression level of PLAGL2 serves as a predictive biomarker for survival in patients with pancreatic ductal adenocarcinoma (PDAC). It is associated with clinical features, including TNM stge, Tumor size, Nerve infiltration, and it also plays a role in promoting epithelial‒mesenchymal transition (EMT) in PDAC, and promotes the proliferation, migration and invasion of PDAC.

Loss of either Drosha or Dicer1 partially mimicked the tumorigenic effects of Rb1 deletion by promoting cell cycle progression through the derepression of Plagl2 and cyclin D2. This work reveals a novel mechanism of pineoblastoma development driven by disrupted miRNA processing and highlights a potential therapeutic strategy targeting downstream proliferative drivers.

One such microRNA target gene is the oncofetal transcription factor Plagl2, which regulates expression of progrowth genes, and inhibiting their signaling impairs tumor growth. Thus, we demonstrate that tumors driven by loss of microRNA processing may be therapeutically targeted by inhibiting downstream drivers of proliferation.

Adjuvant therapy should be considered for all ET, PLAGL patients: Patients with ET, PLAGL2 might benefit from intensified chemotherapy regimens. In contrast, patients with ET, PLAGL1 showed superior outcomes without high-dose chemotherapy or craniospinal irradiation.

Ultimately, the process safeguards GC cells from ferroptosis. These findings elucidate the function of PLAGL2/STAU1/NCOA4 in the ferroptosis of gastric cancer cells and provide theoretical backing for possible diagnostic markers and treatment targets for peritoneal metastasis in gastric cancer.