The diagnostic value and molecular mechanism of exosomal lncGIHCG in prostate cancer

The biological mechanism of exosomal lncGIHCG in prostate cancer (PCa) is unclear. In this study, qRT-PCR detection found that lncGIHCG was highly expressed in cancer tissues, serum exosomes of PCa patients and various human PCa cell lines. Functional experiments showed that knockdown of lncGIHCG could inhibit the proliferation and migration of PCa cells and promote apoptosis, while overexpression of lncGIHCG produced the opposite result. In addition, lncGIHCG enriched in exosomes also had the capacity to modulate the proliferative activity, migratory behavior, and apoptotic rates of PCa cells. Mechanism studies found that lncGIHCG acted as a competitive endogenous RNA (ceRNA) to adsorb miR-181a-5p, relieving its inhibitory effect on the downstream target gene RALBP1, thereby promoting tumor progression. In conclusion, the serum exosomal lncGIHCG may be a potential therapeutic target for prostate cancer. Regulating the lncGIHCG / miR-181a-5p / RALBP1 axis may offer a novel approach for treating prostate cancer. This article studied the expression of exosomal lncGIHCG in prostate cancer (PCa), explored its potential as a biomarker of prostate cancer, the molecular mechanism underlying the role of lncGIHCG in the progression of prostate cancer was analyzed. qRT-PCR was used to detect the presence of GIHCG in cancer tissues and serum exosomes derived from PCa patients, as well as in various human PCa cell lines. GIHCG siRNA and overexpression plasmids were constructed and transfected into different PCa cells to investigate how GIHCG influenced PCa cell proliferation, migratory capacity, and apoptotic rate. PCa cell exosomes were extracted and identified, and the effect of lncGIHCG enriched in exosomes on cell proliferation, migration, and apoptosis was detected. The miRNA that binds to lncGIHCG and its regulatory target gene were predicted through bioinformatics methods, and verified through luciferase reporter gene detection. In the above interaction network, qRT-PCR and Western blot assay were employed to assess the levels of miRNA and its regulatory target gene. LncGIHCG exhibited elevated expression levels in cancer tissues and serum exosomes of PCa patients. By knocking down GIHCG, the formation of cell clones and migration were suppressed, while apoptosis was enhanced. Overexpression of GIHCG produced the opposite result. LncGIHCG enriched in exosomes had the capacity to modulate the proliferative activity, migratory behavior, and apoptotic rates of PCa cells. A binding site existed between lncGIHCG and miR-181a-5p. MiR-181a-5p was low expressed in prostate cancer, and miR-181a-5p mimic could play an anti-cancer role. RALBP1 served as a target gene regulated by miR-181a-5p. Knockdown of RALBP1 could inhibit cell cloning, migration, and promote apoptosis. In addition, knocking down RALBP1 reversed the promotion effect of lncGIHCG overexpression on prostate cancer, demonstrating that lncGIHCG plays a pro-cancer role through the miR-181a-5p/RALBP1 axis. The serum exosomal lncGIHCG may be a potential therapeutic target for prostate cancer. Regulating the lncGIHCG/miR-181a-5p/RALBP1 axis may offer a novel approach for treating prostate cancer.