Long intergenic non-coding RNA 00852 (LINC00852) has been shown to promote the progression of many different cancers including prostate cancer. However, the involved mechanism in promoting the proliferation, migration and invasion of prostate cancer cells has not been reported. In this study, we found that LINC00852 was highly expressed in the tissue of prostate cancer using quantitative reverse transcription PCR (qRT-PCR). CCK-8 assay, colony formation experiment, Transwell migration and invasion experiments were performed to prove that the up-regulation of LINC00852 could promote the proliferation, migration and invasion of prostate cancer cells in vitro. Xenograft tumors experiments in nude mice confirmed that up-regulation of LINC00852 promoted the proliferation of prostate cancer cells in vivo. Bioinformatics predictions and dual-luciferase reporter gene assay showed that miR-29a-3p binds to the 3’-untranslated region of JARID2, and the enhancement of miR-29a-3p could reverse the effect of LINC00852 overexpression in vitro. Moreover, the results of qRT-PCR and western blot showed that LINC00852 could regulate the expression of JARID2 through miR-29a-3p induction. In summary, we demonstrated that LINC00852 played a key role in promoting the prostate cancer, and LINC00852/miR-29a-3p/JARID2 axis could be used as a target for prostate cancer treatment.

Background: Modulation of programmed cell death in tumor cells alters the tumor microenvironment and the influx of tumor-infiltrating lymphocytes, and the combination of its inducers and immune checkpoint inhibitors plays a synergistic role in enhancing antitumor effects.Methods: We downloaded the data of clear cell renal cell carcinoma samples from The Cancer Genome Atlas and used a machine learning approach to build a new programmed cell death index (PCDI) through 13 programmed cell death-related genes. Based on PCDI, clinical features, tumor immune microenvironment, chemotherapy response and immunotherapy response were systematically analyzed.Results: PCDI consists of eight programmed cell death-related genes (TBX3, BID, TCIRG1, IDUA, KDR, PYCARD, IFNG and LRRK2). PCDI is a reliable predictor of survival in clear cell renal cell carcinoma patients and has been validated in multiple external datasets. We found that the high PCDI group showed higher levels of immune cell infiltration and better response to immunotherapy compared to the low PCDI group, and PCDI can also be used for prognostic prediction in a variety of cancers other than clear cell renal cell carcinoma. In vitro experiments demonstrated that knockdown of IDUA inhibited the proliferation and migration of clear cell renal cell carcinoma.Conclusions: The PCDI identified in this study provides valuable insights into the clinical management of clear cell renal cell carcinoma by accurately evaluating the prognosis of patients with clear cell renal carcinoma and identifying the patient population that would benefit from immunotherapy.

Prostate cancer (PCa) is one of the leading causes of cancer-related mortality in men, with castration-resistant prostate cancer (CRPC) posing significant therapeutic challenges due to drug resistance mediated by the androgen receptor (AR) signaling pathway. Indolethylamine-N-methyltransferase (INMT), a tumor-suppressive enzyme downregulated in CRPC, regulates pathways associated with apoptosis and proliferation. Leveraging a structure-based drug design strategy, this study aimed to identify novel INMT agonists for CRPC therapy. Virtual screening of the ChemDiv compound library (guided by the INMT crystal structure, PDB ID: 2A14), combined with molecular docking, MM/GBSA binding energy calculations, and molecular dynamics simulations, identified five candidate compounds. Among these, DMPP-4M stably bound to an allosteric site adjacent to the catalytic domain of INMT via hydrogen bonds, π-cation interactions, and hydrophobic forces. In vitro experiments demonstrated that DMPP-4M dose-dependently upregulated INMT expression, inhibited proliferation, and induced apoptosis in CRPC cell models (PC-3, 22RV1). The mechanism involved activation of the pro-apoptotic protein BAX, suppression of the anti-apoptotic protein Bcl-2, and upregulation of cleaved caspase-3 and PARP. Further mechanistic studies revealed that DMPP-4M-mediated INMT activation suppressed the activity of the TGF-β/Smad and Wnt/β-catenin signaling pathways. These findings suggest that DMPP-4M represents a promising INMT-targeted therapeutic agent, offering an AR-independent strategy for CRPC treatment. Subsequent structural optimization and in vivo experimental validation are required to advance its clinical translation potential.

The cyclic GMPAMP synthase (cGAS) stimulator of interferon genes (STING) pathway is a central component of innate immunity that links cytosolic DNA sensing to type I interferon and NF-κB-driven inflammatory responses. Although transient STING stimulation facilitates antimicrobial defense, tissue remodeling, and tumor immunosurveillance, sustained or maladjusted signaling facilitates chronic sterile inflammation, fibrosis, immune impairment, and carcinogenesis. Mitochondrial injury, cellular senescence, infection-related stress, and DNA damage are caused by STING in epithelial-rich organs like the kidney and prostate, which can cause inflammatory diseases and context-dependent immunomodulation in cancer. This mini-review provides an integrated view of STING activation in renal and prostate tissues, elucidating common mechanistic activators, distinct pathological outcomes, and new translational possibilities. Most recent therapeutic strategies, such as STING agonists to promote antitumor immunity and STING inhibitors to reduce maladaptive inflammation. Further insight into cell-specific and disease-stage-dependent STING regulation will be critical for developing safe and effective interventions to achieve immune homeostasis in renal and prostate pathologies.