Table 1.
Mechanism of Castration Resistance | Subject Investigated (Cell Lines/Tissue) | lncRNA | miRNA | Interactions | Reference | |
---|---|---|---|---|---|---|
AR amplification | 22RV1/human PCa | PlncRNA-1 | miR-34c/miR-297 | PlncRNA-1 promotes AR expression via competitive inhibition of miRNA-34c/miR-297 targeting AR. | [57] | |
Increased AR transcriptional activity | PC3, DU145/human PCa | CCAT1 | miR-28-5P | In cytoplasm: competing for miR-28-5P to promote cell proliferation and colony formation. | [58] | |
In nucleus: CCAT1 acts as a scaffold for DDX5(P68) and AR transcriptional complex to facilitate expression of AR-regulated castration resistance gene (UBE2C). | ||||||
Signal cascades independent of AR and crosstalk with AR | Growth factors | C4-2, PC3, DU145 | AFAP1-AS1 | miR-15b | AFAP1-AS1 upregulates IGF1R by competitively binding with miR-15b to de-repress IGF1R. | [59] |
human PCa | PTTG3P | miR-146a-3p | PTTG3P upregulates PTTG1 to stimulate FGF expression by competing for miR-146a-3p. | [60] | ||
Other oncogenic signal pathways | PC3 | SChLAP1 | miR-198 | SChLAP1 regulates the miR-198 expression and influences cancer progression by the MAPK1 pathway. | [61] | |
human PCa | Linc00963 | miR-655 | Linc00963 competitively binds with miR-655 and upregulates TRIM24 expression to activate the PI3K/AKT pathway. | [62] | ||
PC3, DU145/human PCa | MYU(VPS9D1-AS1) | miR-184 | MYU upregulates the MYC expression by competitively binding with miR-184. | [63] | ||
Cell cycle dysregulation | DU145/human PCa | SNHG7 | miR-503 | MiR-503 targets 3′-UTR of SNHG and inhibits cell cycle proteins (CDK4, CDK6, Cyclin D), inducing G0/G1 cell cycle arrest. | [64] | |
PC3, DU145 | LOXL1-AS1 | miR-541-3p | LOXL1-AS1 interferes with miR-541-3p targeting cell cycle regulator Cyclin D and promotes cell proliferation. | [65] | ||
DU145/human PCa | TTTY15 | let-7 | FOXA1, acting as a transcription factor of TTTY15, promotes PCa progression by sponging let-7 and upregulating CDK6 and FN1. | [66] | ||
Cytokine | C4-2, PC3, DU145 | SNHG17 | miR-144 | SNHG17 acts as a ceRNA to upregulate CD51 (integrin alpha-V) expression through competitively sponging miR-144. | [67] | |
Unidentified mechanisms | PC3, DU145 | HOTAIR | miR-34a | MiR-34a directly targets HOTAIR and inhibits cell growth. | [68] | |
PC3 | HOTAIR | miR-193a | HOTAIR couples with EZH2 to repress miR-193a by trimethylation of H3K27me3; miR-193a directly targets HOTAIR to reduce HOTAIR level in miR-193a overexpressed cells. | [69] | ||
PC3 | PCGEM-1 | miR-148a | Putative PCGEM1 binding site is identified in the 5′-UTR of miR-148a; PCGEM-1 expression represses miR-148a and cell apoptosis. | [70] | ||
PC3, DU145/human PCa | PCSEAT | miR-143-3p-/miR-24-2-5p | PCSEAT competitively sponges miR-143-3p/miR-24-2-5p and decreases PCSEAT-mediated cell proliferation. | [71] | ||
PC3, DU145/human PCa | Linc00308 | miR-137 | LncRNA-miRNA-mRNA networks regulate tumor suppressor gene PTGS2 and DUSP2 and affect survival. | [72] | ||
Linc00355 | miR-122/miR-506 | |||||
OSTN-AS1 | miR-137/miR-506 |
AR: Androgen receptor; FGF: fibroblast growth factor; FN1: fibronectin; IGF1R: insulin-like growth factor 1 receptor; PCa: prostate cancer; ceRNA: competing endogenous RNA.