Go-Ichi-Ni-San 2: A potential biomarker and therapeutic target in human cancers

Cancer incidence and mortality are increasing globally, leading to its rising status as a leading cause of death. The Go-Ichi-Ni-San (GINS) complex plays a crucial role in DNA replication and the cell cycle. The GINS complex consists of four subunits encoded by the GINS1, GINS2, GINS3, and GINS4 genes. Recent findings have shown that GINS2 expression is upregulated in many diseases, particularly tumors. For example, increased GINS2 expression has been found in cervical cancer, gastric adenocarcinoma, glioma, non-small cell lung cancer, and pancreatic cancer. It correlates with the clinicopathological characteristics of the tumors. In addition, high GINS2 expression plays a pro-carcinogenic role in tumor development by promoting tumor cell proliferation and migration, inhibiting tumor cell apoptosis, and blocking the cell cycle. This review describes the upregulation of GINS2 expression in most human tumors and the pathway of GINS2 in tumor development. GINS2 may serve as a new marker for tumor diagnosis and a new biological target for therapy.     

啤酒制造工人工作相关肌肉骨骼疾患及其影响因素分析

目的 调查啤酒制造工人工作相关肌肉骨骼疾患（WMSDs）的现状并探讨其影响因素。方法 采用流行病学横断面调查方法，选择广州市某大型啤酒制造厂501名啤酒制造工人为研究对象，应用中文版《肌肉骨骼疾患调查问卷》调查WMSDs的患病现状，采用多因素Logistic回归方法分析工人罹患WMSDs的影响因素。结果 啤酒制造工人WMSDs总发生率为39.7%（199/501），其中发生率较高的部位是颈部27.1%（136/501）、肩部25.0%（125/501）、下背部24.0%（120/501）、上背部23.2%（116/501）。啤酒制造工人罹患多部位WMSDs的比例为28.9%（145/501），单一部位发生率为10.8%（54/501）。多因素Logistic回归分析结果显示，与总工龄<5年者相比，工龄10～<15年的工人罹患WMSDs的风险增加（P<0.05）；吸烟≥20支/周、经常替同事上班者罹患WMSDs的风险增加（P<0.05）。结论 啤酒制造工人WMSDs患病风险较高，发生率较高的部位分别是颈部、肩部和下背部。啤酒制造行业应加强员工健康培训，注意对工龄较长员工的保护，宣传吸烟危害，合理安排工人轮休和作息，以降低工人罹患WMSDs的风险。     

Small nucleolar RNA host gene 3 functions as a novel biomarker in liver cancer and other tumour progression

Cancer has become the most life-threatening disease in the world. Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs, especially long noncoding RNAs (lncRNAs), have significant effects in human cancers. LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes. Small nucleolar RNA host gene 3 (SNHG3) is a novel lncRNA and has been reported to be differentially expressed in various tumors, such as liver cancer, gastric cancer, and glioma. However, the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood. In this review, we summarize the results of SNHG3 studies in humans, animal models, and cells to underline the expression and role of SNHG3 in cancer. SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis. SNHG3 expression in lung adenocarcinoma remains controversial. Concurrently, SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms, including competing endogenous RNA effects. A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.     

SLC12A5 interacts and enhances SOX18 activity to promote bladder urothelial carcinoma progression via upregulating MMP7

Solute carrier family 12 member 5 (SLC12A5) has an oncogenic role in bladder urothelial carcinoma. The present study aimed to characterize the molecular mechanisms of SLC12A5 in bladder urothelial carcinoma pathogenesis. Functional assays identified that in bladder urothelial carcinoma SLC12A5 interacts with and stabilizes SOX18, and then upregulates matrix metalloproteinase 7 (MMP7). In vivo and in vitro assays were performed to confirm the effect of SLC12A5’s interaction with SOX18 on MMP7‐mediated bladder urothelial carcinoma progression. SLC12A5 was upregulated in human bladder tumors, and correlated with the poor survival of patients with bladder urothelial carcinoma tumor invasion and metastasis, promoted by SLC12A5 overexpression. We demonstrated that SLC12A5 interacted with SOX18, and then upregulated MMP7, thus enhancing tumor progression. Importantly, SLC12A5 expression correlated positively with SOX18 and MMP7 expression in bladder urothelial carcinoma. Furthermore, SLC12A5 expression was suppressed by miR‐133a‐3p. Ectopic expression of SLC12A5 partly abolished miR‐133a‐3p‐mediated suppression of cell migration. SLC12A5‐SOX18 complex‐mediated upregulation on MMP7 was important in bladder urothelial carcinoma progression. The miR‐133a‐3p/SLC12A5/SOX18/MMP7 signaling axis was critical for progression, and provided an effective therapeutic approach against bladder urothelial carcinoma.     

肺鳞癌治疗新靶点FGFR的研究进展

肺癌是目前全球发病率和死亡率均居前列的恶性肿瘤，其中肺鳞癌经手术、放化疗等综合治疗后，其疗效仍不满意。随着分子靶向治疗在肺腺癌中取得了令人瞩目的成果，而肺鳞癌患者中EGFR基因突变及ALK融合基因少见，急需探索新的靶点指导肺鳞癌患者的临床治疗。研究表明，FGFR家族（FGFR1-4）是肺鳞癌中突变频率较高的基因，FGFR基因的激活突变和扩增与肺鳞癌的发生和发展密切相关，同时许多小分子 FGFR 抑制剂在临床应用中已经取得较好的治疗效果。目前，许多FGFR抑制剂治疗肺鳞癌的临床试验也正在进行研究，针对FGFR靶点的基因治疗可为肺鳞癌的治疗提供一种新的策略。本文就FGFR在肺鳞癌的靶向治疗中的最新研究进展进行综述。     

黄精属药食两用中药玉竹与黄精的比较

玉竹与黄精是黄精属的2种代表性药食两用中药,食疗价值突出。然而本属植物形态较为相似,分类和鉴定困难,导致玉竹与黄精的民间习用品较多,来源混杂。长期以来玉竹与黄精的保健食品开发处于不平衡状态,玉竹的食疗价值及应用被忽视。因此,从玉竹与黄精的形态差异、功效演变和古今食用情况进行比较分析,并提出今后的发展建议,以期为两者的开发应用提供参考。     

超高CD34+采集的动员方案序贯二次自体造血干细胞移植治疗难治性 霍奇金淋巴瘤

目的:探讨超高CD34+采集的动员方案后序贯二次自体造血干细胞移植治疗难治性霍奇金淋巴瘤的疗效和安全性。方法:对1例经过多疗程一线、二线、新药、免疫等均难治的霍奇金淋巴瘤患者，予以IA+C方案化疗+G-CSF动员干细胞后采集出超高水平CD34+细胞，之后行自体造血干细胞移植，移植后获得完全缓解，再予序贯第二次自体造血干细胞移植进行巩固治疗。结果:总计输注单个核细胞数13.67×108/kg，CD34+细胞48.68×106/kg，第一次自体造血干细胞移植术后第7天造血功能恢复，复查全身PET-CT提示获得完全缓解，第二次自体造血干细胞移植术后第8天造血功能恢复，两次自体造血干细胞移植相关并发症均在可控范围内。结论:超高CD34+细胞采集的IA+C方案化疗+G-CSF动员可以让患者有机会进行多次自体造血干细胞移植，是临床动员的创新方案。对于难治性霍奇金淋巴瘤，序贯二次自体造血干细胞移植可达到更深层次缓解，且安全性较高，延长患者无疾病生存期及总生存期，为难治性霍奇金淋巴瘤治疗提供更多临床依据。