摘要: Scoliosis, a complex three-dimensional deformity of the spine with the Cobb angle (a measure of the spinal lateral curvature) >10 degree, encompasses a spectrum of pathologies, including congenital, idiopathic, syndromic and neuromuscular aetiologies. The pathogenesis is multifactorial involving both environmental and genetic factors but the exact cellular and molecular mechanisms of disease development remain largely unknown. Emerging evidence showed that non-coding RNAs (ncRNAs), namely microRNAs, long ncRNAs and circular RNAs, are deregulated in many orthopaedic diseases, including scoliosis. Importantly, these deregulated ncRNAs functionally participate in the initiation and progression of scoliosis. Here, we review recent progress in ncRNA research on scoliosis.

摘要: Objective The long non-coding RNA zinc finger E-box-binding homeobox 1 antisense 1 (ZEB1-AS1) acts as an oncogenic regulator in many human tumours. In the present study, we identify the role and potential molecular biological mechanisms of ZEB1-AS1 in colon adenocarcinoma (COAD). Methods QRT-PCR was used to detect the expression of ZEB1-AS1, miR-455-3p and p21-activated kinases 2 (PAK2) in COAD tissues. CCK8 assay, EdU assay, transwell assay and scratch wound assay were used to explore the biological function of ZEB1-AS1 in COAD cells. Bioinformatics, luciferase reporter assays and an RNA pull-down assay were used to demonstrate the mechanism of ZEB1-AS1. We further explore the role of ZEB1-AS1 in vivo though xenograft tumour assay. Results We found that ZEB1-AS1 expression was significantly up-regulated in COAD tissues, and high ZEB1-AS1 level was correlated with the poor prognosis of COAD patients. MiR-455-3p plays an anti-cancer role in COAD by targeting PAK2. We confirmed that ZEB1-AS1 promotes PAK2 expression by sponging miR-455-3p, thus facilitating COAD cell growth and metastasis. Conclusions To sum up, this result illustrates the novel molecular mechanism of ZEB1-AS1 in COAD and provides a new target for the diagnosis and treatment of COAD patients.

摘要: Objectives To detect folate receptor (FR)-positive circulating tumour cells (FR+CTCs) by using ligand-targeted polymerase chain reaction (LT-PCR) in periampullary cancer patients and to investigate the diagnostic value of FR+CTCs in distinguishing pancreatic cancer (PC) from benign pancreatic disease. Materials and Methods CTCs were enriched from 3 mL of peripheral blood and portal vein blood by immunomagnetic depletion of leucocytes and were then detected by LT-PCR. The diagnostic performance of FR+CTCs in PC was investigated by receiver-operating characteristic curve analysis. Results In total, 57 consecutive patients, including 46 patients with PC, five patients with non-pancreatic periampullary cancer (non-PC) and six patients with benign pancreatic diseases, were enrolled. FR+CTC levels were significantly higher in patients with malignant diseases (PC and non-PC) than in patients with benign pancreatic diseases (P < .01). There was no notable difference in CTC levels between patients with PC and those with non-PC (P > .05). The combination of FR+CTCs with carbohydrate antigen 19-9 (CA19-9) had better diagnostic efficiency than each of these two markers alone, with high sensitivity (97.8%) and specificity (83.3%). Conclusions LT-PCR is feasible and reliable for detecting FR+CTCs in patients with periampullary cancer. FR+CTCs, especially when used in combination with CA19-9, have potential as a biomarker for the diagnosis of PC.

摘要: Hepatocellular carcinoma (HCC) is a primary liver malignancy with a high global prevalence and a dismal prognosis. Studies are urgently needed to examine the molecular pathogenesis and biological characteristics of HCC. Chromatin remodelling, an integral component of the DNA damage response, protects against DNA damage-induced genome instability and tumorigenesis by triggering the signalling events that activate the interconnected DNA repair pathways. The SWI/SNF complexes are one of the most extensively investigated adenosine triphosphate-dependent chromatin remodelling complexes, and mutations in genes encoding SWI/SNF subunits are frequently observed in various human cancers, including HCC. The mutated SWI/SNF complex subunits exert dual functions by accelerating or inhibiting HCC initiation and progression. Furthermore, the abnormal SWI/SNF complexes influence the transcription of interferon-stimulated genes, as well as the differentiation, activation and recruitment of several immune cell types. In addition, they exhibit synergistic effects with immune checkpoint inhibitors in the treatment of diverse tumour types. Therefore, understanding the mutations and deficiencies of the SMI/SNF complexes, together with the associated functional mechanisms, may provide a novel strategy to treat HCC through targeting the related genes or modulating the tumour microenvironment.

摘要: Objectives CD31(hi)EMCN(hi) vessels (CD31, also known as PECAM1 [platelet and endothelial cell adhesion molecule 1]; EMCN, endomucin), which are strongly positive for CD31 and endomucin, couple angiogenesis and osteogenesis. However, the role of CD31(hi)EMCN(hi) vessels in bone regeneration remains unknown. In the present study, we investigated the role of CD31(hi)EMCN(hi) vessels in the process of bone regeneration. Materials and Methods We used endothelial-specific Kruppel like factor 3 (Klf3) knockout mice and ophiopogonin D treatment to interfere with CD31(hi)EMCN(hi) vessel formation. We constructed a bone regeneration model by surgical ablation of the trabecular bone. Immunofluorescence and micro-computed tomography (CT) were used to detect CD31(hi)EMCN(hi) vessels and bone formation. Results CD31(hi)EMCN(hi) vessels participate in the process of bone regeneration, such that endothelial-specific Klf3 knockout mice showed increased CD31(hi)EMCN(hi) vessels and osteoprogenitors in the bone regeneration area, and further accelerated bone formation. We also demonstrated that the natural compound, ophiopogonin D, acts as a KLF3 inhibitor to promote vessels formation both in vitro and in vivo. Administration of ophiopogonin D increased the abundance of CD31(hi)Emcn(hi) vessels and accelerated bone healing. Conclusions Our findings confirmed the important role of CD31(hi)Emcn(hi) vessels in bone regeneration and provided a new target to treat bone fracture or promote bone regeneration.