Objective The purpose of this research was to investigate the outcomes between unilateral biportal endoscopic discectomy (UBE) and percutaneous endoscopic lumbar discectomy (PELD) for the single L4/5‐level lumbar disk herniation (sLDH). Methods From January 2018 to January 2021, a total of 40 patients with sLDH were retrospectively analyzed in this study. All the patients had received spinal surgeries in Affiliated Hospital of Nantong University and Affiliated Nantong Hospital 3 of Nantong University. Among them, 20 patients were treated with PELD (PELD group), and 20 patients were treated with UBE discectomy (UBE group). Postoperative length of hospital stay, estimated blood loss, operation time, and clinical complications of the patients were compared between the two groups. The visual analog scale (VAS) and Oswestry Disability Index (ODI) were measured before surgeries and 3 days, 1, and 6 months after surgeries. Results Compared with the UBE group, the PELD group had obviously less intraoperative blood loss, shorter operative time, and shorter hospital stay. The differences in the rate of complications were not statistically significant between the two groups. The VAS score and the ODI score of the two groups had a great reduction after operation. In addition, both the groups had satisfactory clinical outcome; the VAS score and ODI of the PELD group decreased more obviously. Conclusion The UBE for sLDH yielded similar clinical outcomes to PELD as minimally invasive surgeries; however, PELD is superior to UBE in terms of intraoperative blood loss, operative time, postoperative hospitalization, and short‐term postoperative pain relief. The advantages and disadvantages of the two surgeries should be circumspectly balanced when evaluating a patient for a minimally invasive surgery for sLDH, selecting the most appropriate surgical method for patients.
Intervertebral disc degeneration (IDD) is a leading cause of degenerative spinal disease. Long non-coding RNA (lncRNA) LINC00284 is overexpressed in multiple types of cancer and promotes cancer cell proliferation and inhibits apoptosis; however, its role in human IDD and nucleus pulposus (NP) remain unclear. In the present study, intervertebral disc (IVD) tissues were collected from IDD patients for detection of LINC00284 expression using reverse transcription-quantitative PCR, the binding effect between miR-205-3p and LINC00284 was validated by dual-luciferase reporter assay. miR-205-3p and small interfering RNA (siRNA) was used for LINC00240 knockdown to investigate the proliferation, apoptosis of cells in the NP cells measured by Cell Counting Kit (CCK)-8 assay and Annexin V-FITC/Propidium Iodide (PI) staining with flow cytometry receptivity. IDD animal models were constructed for in vivo study of the role LINC00284 in IDD improvement. The results showed that LINC00284 expression was upregulated in IDD tissue and IL-1β-induced NP cells. LINC00284 knockdown resulted in an increase in IL-1β-induced NP cell proliferation, a decrease in apoptosis and matrix metalloproteinase-3 expression and an increase in expression of extracellular matrix (ECM) markers aggrecan and collagen II. In vivo experiments and histomorphometric analysis confirmed the protective effect of LINC00284 knockdown in IDD. LINC00284 was also shown to be a target of microRNA (miR)-205-3p, and there was a negative correlation between LINC00284 and miR-205-3p levels in IDD tissue. Additionally, LINC00284 knockdown or miR-205-3p upregulation resulted in inhibition of Wnt/β-catenin signaling and subsequent degradation of the ECM. The present study demonstrated that LINC00284 activated the Wnt/β-catenin signaling via sponging miR-205-3p, resulting in inhibition of NP cell proliferation and ECM synthesis. These results suggested that targeting LINC00284 to rescue miR-205-3p expression may be a potential method for IDD management.
Background Osteosarcoma is a malignant tumor originating from the skeletal system. There is no effective treatment other than surgery and chemotherapy, which seriously endangers the health of children and adolescents. NEK6 is a novel discovered Serine/Threonine protein kinase that can regulate cell cycle and activate several oncogenic pathways. Methods NEK6 expression in pan-cancer including sarcoma was evaluated using analysis tools of TIMER, UALCNA and GEPIA with TCGA database, and its association with overall survival in patients with sarcoma was also analyzed. TargetScan, tarbase, microT-CDS and Starbase online software were used to predict NEK6-targeted miRNAs, including miR-26a-5p. Tumor tissues from patients with osteosarcoma were collected for NEK6 and miRNA detection using RT-qPCR. NEK6 down-regulated by siRNAs or miR-26a-5p in osteosarcoma cells was detected by RT-qPCR, Western blot and Immunofluorescence staining assays. Effects of NEK6 knockdown on proliferation, migration, invasion and apoptosis of osteosarcoma cells were detected by CCK-8, wound healing, transwell and flow cytometry, respectively. The expressions of STAT3, metastasis and apoptosis-related genes were detected by Western blot. Results High expression of NEK6 and low expression of miR-26a-5p were lowly expressed in osteosarcoma and they were negative correlation. NEK6 has been confirmed as a direct target for miR-26a-5p. In addition, NEK6 down-regulated by siRNAs or miR-26a-5p led to inhibition of cell proliferation, migration and invasion while promoting cell apoptosis. The levels of phosphorylated STAT3 and metastasis genes (MMP-2, MMP-9) were inhibited, while apoptotic gene Bax was promoted and Bcl2 was inhibited by miR-26a-5p upregulation. Conclusion NEK6 can promote osteosarcoma progression via activating STAT3 signaling pathway, which is inhibited by miR-26a-5p, suggesting that NEK6 is a potential oncogene and miR-26a-5p is a suppressor of osteosarcoma. The strategy of inhibiting of NEK6 by miR-26a-5p may be an effective approach for osteosarcoma therapy.
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