PELP1 (Proline, Glutamate And Leucine Rich Protein 1)

PELP1's structural motifs, unique scaffolding function, and oncogenic activity make it a potential target for a range of therapeutic approaches. This review summarizes the most recent advancements in PELP1 biology, with a particular focus on the emergent oncogenic functions of PELP1 and its inhibitors for the treatment of cancer.

Overexpression of NFE2L1-DT or ALKBH5, or silencing Cx43, attenuated the protective effects of IRF1 silencing against radiation-induced damage. These findings indicate that radiation-induced IRF1 upregulation leads to endothelial injury by promoting pyroptosis through the NFE2L1-DT/ALKBH5/Cx43 axis.

PELP1 promotes EOC progression by enhancing cellular proliferation, metastasis and angiogenesis through the regulation of VEGFA. These findings suggest that PELP1 could serve as a potential therapeutic target for EOC.

This suggests that the relationship between these miRNAs and the selected genes is context-specific. Our findings suggest that hsa-miR-21-5p and hsa-miR-145-5p expression levels may be prognostic or diagnostic markers for ovarian cancer patients.

Importantly, SMIP34, a first-in-class small molecule inhibitor targeting PELP1, effectively decreased the cell viability, clonogenic survival and invasiveness of HCC cells...Further, the knockdown or pharmacological inhibition of PELP1 significantly decelerated the HCC tumor growth in xenograft models. In summary, our study findings indicate that PELP1 could serve as a promising target for therapeutic intervention in HCC.

Importantly, SMIP34 treatment resulted in a significant reduction of the growth of ECa xenografts. Collectively, these findings underscore the potential of SMIP34 in treating ECa.

The AR-interactors might be useful markers for prostate cancer diagnosis and prognosis, and provide a new sight for revealing the molecular mechanism of CRPC progression.

Together, these findings from in vitro, ex vivo, and in vivo models show that SMIP34 may be a useful therapeutic agent for inhibiting PELP1 signaling in TNBC.

This review describes the mechanisms of targeted-drug resistance and newly identified non-small cell lung cancer targets (e.g., KRAS G12C, NGRs, DDRs, CLIP1-LTK, PELP1, STK11/LKB1, NFE2L2/KEAP1, RICTOR, PTEN, RASGRF1, LINE-1, and SphK1). Research into these mechanisms and targets will drive individualized treatment of non-small cell lung cancer to generate better outcomes.

Silencing significantly inhibited lung cancer cell proliferation, migration, and invasion (P < 0.05) and promoted high sensitivity of lung cancer cells to tyrosine kinase inhibitor (TKI) gefitinib...Furthermore, the number of T regulatory cell was higher in lung adenocarcinoma with pelp1 high-expression and pelp1 expression was negatively correlated with CD274 (PDL-1) and CTLA4. Therefore, PELP1 plays an important role in the malignant behavior of NSCLC and could be a potential therapeutic target.