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Objective:To investigate the correlation between the expression level of serum exosome miR-29C and postoperative cognitive dysfunction (POCD) in elderly patients undergoing surgery.Methods:A total of 119 elderly patients who underwent elective spinal surgery in the Second Hospital of Shanxi Medical University from January 2021 to January 2022 were selected and scored on the Montreal Cognitive Assessment (MoCA) Scale 1 day before surgery and 1, 7 and 21 days after surgery. The selected patients were divided into POCD group (51 cases) and non-POCD group (68 cases) according to whether the MoCA Scale score decreased ≥2 points 1 day before surgery and 1 day after surgery. S100-β, neuron-specific enolase (NSE) levels and serum exosome miR-29C expression levels were detected and analyzed in all patients 1 day before and 1 day after surgery. Pearson correlation analysis showed the correlation between MoCA Scale score and S100-β, NSE and miR-29C. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value of S100-β, NSE and miR-29C for POCD occurrence in elderly patients undergoing surgery.Results:The score of MoCA Scale in POCD group were significantly decreased 1, 7 and 21 days after surgery compared with 1 day before surgery (all P<0.05), while the score of MoCA Scale in non-POCD group were significantly decreased only 1 day after surgery compared with 1 day before surgery ( P<0.05). The levels of S100-β and NSE and the expression level of serum exosome miR-29C in 2 groups were significantly increased 1 day after surgery compared with 1 day before surgery (all P<0.05). Moreover, the levels of S100-β and NSE and the expression level of serum exosome miR-29C in POCD group were significantly higher than those in non-POCD group 1 day after surgery (all P<0.05). There was a negative correlation between the MoCA Scale score and the expression level of serum exosome miR-29C 1 day after surgery in the POCD group ( P<0.05). ROC curve analysis showed that the expression levels of NSE, S100-β and exosome miR-29C 1 day after surgery predicted the risk of POCD in elderly surgical patients with area under the curve (AUC) of 0.891, 0.908 and 0.918, respectively. Conclusions:The occurrence of POCD in elderly patients with surgery is related to the increase of the expression level of serum exosome miR-29C, and the expression level of serum exosome miR-29C is negatively correlated with MoCA Scale score. Early monitoring of the miR-29C expression level can provide a basis for the occurrence and development of postoperative POCD in elderly patients, disease diagnosis and clinical intervention.
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OBJECTIVE@#To investigate the mechanism by which long non-coding RNA TUG1 affects bladder cancer cell migration and invasion.@*METHODS@#The expressions of TUG1 and miR-29c-3p were examined by quantitative RT-PCR (qRT-PCR) in 10 bladder cancer tissues and 5 bladder cancer cell lines. Trans-well assay was used to detect the changes in migration and invasion abilities of bladder cancer T24 cells after TUG1 knockdown using RNA interference technique, and the alteration in the expression of CAPN7 was also detected. The expression of CAPN7 was examined in T24 cells overexpressing mir-29c-3p by Western blotting, and luciferase reporter assay was performed to confirm the targeting of miR-29c-3p to TUG1 and CAPN7. The effects of CAPN7 overexpression and sh-TUG1 on the migration and invasion of T24 cells were investigated.@*RESULTS@#The expression of TUG1 was up-regulated and mir-29c-3p was down-regulated significantly in bladder cancer tissue with a negative correlation between their expressions. TUG1 knockdown significantly inhibited the migration and invasion of T24 cells ( < 0.01). Overexpression of mir-29c-3p in T24 cells obviously down-regulated the expression of CAPN7 protein, whose expression was positively correlated with TUG1 expression (=0.4081, =0.0139). The results of luciferase reporter assay confirmed both TUG1 and CAPN7 as the targets of mir-29c-3p. CAPN7 overexpression could partially reverse the tumor suppressing effect of sh-TUG1 in T24 cells.@*CONCLUSIONS@#Mir-29c-3p targeting TUG1 affects the migration and invasion of bladder cancer cells by regulating the expression of CAPN7.
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Objective To investigate the effect of miR-29c on radiosensitivity of hepatoma HepG2 cells by targeting AKT2 gene.Methods The expression of miR-29c in human normal hepatocytes THLE-3 and hepatoma cell HepG2 was detected by RT-PCR.The relationship between miR-29c and AKT2 were predicted by predicted by informative analysis and verified by dual luciferase reporter gene test and Western blot.miR-29c mimic/AKT2 gene recombinant plasmid and miR-29c inhibitor/ lentivirus vector AKT2 shRNA were transfected into HepG2 cells by Liposome 2000.The cells were irradiated with different doses (0,2,4,6 and 8 Gy) of X-rays,and the effects of miR-29/AKT2 on the survival and cell viability of HepG2 cells were detected by cloning and MTT assays.Results Compared with THLE-3 cells,the expression of miR-29c in HepG2 cells was significantly lower (t=17.816,P＜0.05).After 2,4,6 and 8 Gy X-ray irradiation,the survival of HepG2 cells was significantly lower than that of THLE-3 cells (t =4.541,6.823,7.218,9.363,P＜0.05),and the expression of miR-29c in HepG2 cells was significantly decreased (t =5.599,9.262,10.470,10.873,P＜0.05).The survival and viability of HepG2 cells were decreased by miR-29c overexpression (tsurvival rate =4.307,7.668,7.668,6.894,P＜0.05;tcell viability =3.443,8.116,13.434,P ＜ 0.05) but they were increased by miR-29c inhibition (tsurvival rate =4.003,6.713,7.141,P＜0.05;tcell viability =4.282,5.113,P＜0.05).Double luciferase reporter gene experiments showed that AKT2 was the target gene of miR-29c since the expression of AKT2 was negatively regulated by miR-29c.After the silence of AKT2 or overexpression of AKT2,the survival and viability of HepG2 cells were consistent with the overexpression of miR-29c or the inhibition of miR-29c,respectively.Conclusions MiR-29c increases the radiosensitivity of hepatoma cell HepG2 by targeting AKT2.
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@# Objective: To investigate the mechanism of miR-29c modulating apatinib resistance of gastric cancer tissues and cells MGC-803 via regulating TNRC18. Methods: A total of 39 gastric cancer patients with complete clinical data, who were treated in the Central Hospital of Wuhan from Feb. 2015 to Oct. 2017, were collected for this study. The expression of miR-29c was detected by qRTPCR in gastric cancer tissues and cell lines. The effect of miR-29c over-expression/knockdown on the proliferation, invasion and apoptosis of MGC-803/AP cells in vitro was measured by CCK-8 assay, Transwell and Annexin V-FITC/PI double staining flow cytometry assay. Western blotting was used to detect the regulation of miR-29c on TNRC18. Moreover, the relationship between miR-29c and TNRC18 was examined by dual luciferase reporter gene assay. Results: qRT-PCR revealed that miR-29c was low expressed in gastric cancer cell lines and gastric cancer tissues from patients resistant to apatinib. Moreover, dual luciferase reporter gene assay confirmed that miR-29c directly binds to the 3′UTR of TNRC18 mRNAto suppress its expression in MGC-803/AP cells. Furthermore, miR-29c inhibited the apatinib resistance in gastric cancer MGC-803/AP cells via inhibiting cell proliferation, invasion and promoting cell apoptosis by targeted down-regulating TNRC18. Additionally, in vivo experiment also confirmed that miR-29c modulated apatinib-resistance in gastric cancer cells by targeted inhibiting TNRC18. Conclusion: miR-29c/TNRC18 axis plays a certain role in the resistance of gastric cancer tissues and MGC-803/AP cells to apatinib, and over-expression of miR-29c may reverse the resistance of MGC-803/AP cells to apatinib.
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Objective To study the effect of miR-29c on the apoptosis of prostate cancer cell line PC 3.Methods The expression of miR-29c, VEGF and VEGFR2 in RWPE-1 and PC3 were detected to verify the different between normal and cancer cell .The location of p-VEGFR2 was measured by immunofluorescence (IF).After PC3 cell were transfected by miR-29c overexpression adenovirus , the expression level of miR-29c, VEGF, t-VEGFR2, p-VEGFR2, BAX and Bcl-2 were measured by RT-PCR and Western blot , the cell apoptosis rate was detected by the kits of ho-echst 33258 and FCM.Results The expression level of miR-29c was lower and VEGF, VEGFR2 was higher in PC3 cell compared with that in RWPE-1(P<0.001).The expression level of miR-29c and BAX were higher and VEGF , p-VEGFR2 and Bcl-2 were lower in Ad-miR-29c group compared with that in control group (P<0.001).Higher apop-tosis rate was detected in Ad-miR-29c group compared with control group (P<0.001).Conclusions miR-29c can promote apoptosis in prostate cancer cell PC 3 by significantly inhibiting VEGF/VEGFR2 signaling.
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Objective To investigate the expression of miR-29s in the glioma stem cells,and explore how the members of miR-29s affect the bio-logical behaviors of glioma stem cells. Methods Eight patient specimens were used to culture glioma stem cells. Real-time PCR was adopted to test the expression of miR-29s. CCK-8 analysis was performed to test the proliferation ,Transwell was used to test cell migration and invasion ,and flow-cytometry analysis was carried out to test apoptosis. Results miR-29a,miR-29b and miR-29c were decreased in glioma stem cells. Over-ex-pression of miR-29s could inhibit the proliferation,cell migration and invasion,but promote apoptosis of glioma stem cells. Conclusion miR-29s acts as a cancer suppressor gene in the glioma stem cells ,and miR-29a plays the dominant functional role in the family.
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Objedive To observe the effect of microRNA-29c cm the proliferalion and invasion abililies of hirman prostate carreer cell litre LNCaP, and to discijss its potetrlial applicasion. Methods The difference in miR-29c expression between ADPC (androgen-dependent prostate cancer) and AIPC (androgen-independent prostate cancer)cell lines was observed by real time RT-PCR.MiR-29c-inhibitor (anti-miR-29c) was used to decrease miR-29 cexpression in LNCaP cells; then the cell proliferation was examined with CCK-8 assay, the cell cycle was analyzed using flow cytometry, and the invasive abilities of LNCaP cells were observed by transwell invasion assay before and after treatment with anti-miR-29c.Results The result of real-timeRT- PCR showed that miR-29c expression in LNCaP-AI cells was significantly lower than that in LNCaP cells (P<0.05).Down- expression of miR-29c in LNCaP cells significantly promoted the proliferation and invasion abilities of LNCaP cells (P<0.05). Conclusion Normal expression of miR-29c plays an inhibitory role in the proliferation and invasion of LNCaP cells, in dicating it might be a new target for biotherapy of prostate cancer.