Micro-RNA-204 Participates in TMPRSS2/ERG Regulation and Androgen Receptor Reprogramming in Prostate Cancer.

Cancer progression is driven by genome instability incurred rearrangements such as transmembrane protease, serine 2 (TMPRSS2)/v-ets erythroblastosis virus E26 oncogene (ERG) that could possibly turn some of the tumor suppressor micro-RNAs into pro-oncogenic ones. Previously, we found dualistic miR-204 effects, acting either as a tumor suppressor or as an oncomiR in ERG fusion-dependent manner. Here, we provided further evidence for an important role of miR-204 for TMPRSS2/ERG and androgen receptor (AR) signaling modulation and fine tuning that prevents TMPRSS2/ERG overexpression in prostate cancer.

Sertoli cells have a functional NALP3 inflammasome that can modulate autophagy and cytokine production.

Sertoli cells, can function as non-professional tolerogenic antigen-presenting cells, and sustain the blood-testis barrier formed by their tight junctions. The NOD-like receptor family members and the NALP3 inflammasome play a key role in pro-inflammatory innate immunity signalling pathways. Limited data exist on NOD1 and NOD2 expression in human and mouse Sertoli cells.

miR-204 is dysregulated in metastatic prostate cancer in vitro.

During cancer progression, the genome instability incurred rearrangement could possibly turn some of the tumor suppressor micro-RNAs into pro-oncogenic ones. We aimed to investigate miR-204 in the context of prostate cancer progression using a cell line model of different levels of genome instability (LNCaP, PC3, VCaP and NCI H660), as demonstrated by the availability of ERG fusion. We studied the effect of miR-204 modulation on master transcription factors important for lineage development, cell differentiation and prostate cancer bone marrow metastasis.

Fundamental role of microRNAs in androgen-dependent male reproductive biology and prostate cancerogenesis.

Male reproductive failure has been linked to successive development of various urologic diseases including prostate cancer. There is strong epidemiologic data in support of this association, it is important therefore to identify the fundamental grounds that lay beneath such a connection. Male reproductive biology, as sex determined, is significantly dependent upon the hormonal regulation of androgens.

Immunosurveillance and immunoediting--can the immune response be made more "immunodemocratic"?

Increasing evidence has demonstrated that the immune system is able to mount responses against tumors and that these responses can be enhanced using a number of strategies. Several of these strategies are currently being evaluated in clinical trials, where their efficacy and cost effectiveness will be ascertained. Sadly, we have to admit that despite great expectations and enormous achievements in basic immunology and molecular biology, immunotherapeutic interventions relying on the elicitation of cytotoxic cellular immunity so far have had limited success.