Background: Oesophageal cancer (OC) is the sixth leading cause of cancer death worldwide. Despite the improvement of therapeutic methods in recent years, the prognosis of OC remains unsatisfactory. Kang-ai injection, a kind of traditional Chinese herbal medicine, has been widely applied as a promising adjunctive drug for OC. In this study, we aimed to summarize the efficacy and safety of Kang-ai injection for patients with advanced OC through the meta-analysis, in order to provide scientific reference for the design of future clinical trials. Methods: Relevant randomized controlled trials and high-quality prospective cohort studies were searched from PubMed, Web of Science, Medline, Cochrane Library, Google Scholar, Excerpt Medica Database, Chinese Biomedical Literature Database, China National Knowledge Infrastructure, China Scientific Journal Database and Wanfang Database. Papers in English or Chinese published from their inception to August 2020 will be included without any restrictions. Study selection and data extraction will be performed independently by 2 investigators. The clinical outcomes including overall response rate, disease control rate, overall survival, disease-free survival, quality of life, immune function and adverse events, were systematically evaluated. Stata 14.0 and Review Manager 5.3 were used for data synthesis, subgroup analysis, sensitivity analysis, meta regression, and risk of bias assessment. Results: The results of this study will be published in a peer-reviewed journal, or presented the findings at a relevant conference. Conclusion: Our study will draw an objective conclusion of the effects of Kang-ai injection combined with conventional treatment for advanced OC and provide a helpful evidence for clinicians to formulate the best postoperative adjuvant treatment strategy for OC patients. INPLASY registration number: INPLASY202080019.

Esophageal cancer (EC) is one of the most lethal malignancies in humans, and multiple miRNAs have been identified to modulate EC progression by targeting different targets. However, the effect and related mechanism of microRNA-33a-5p (miR-33a-5p) on EC development remain elusive. In this study, we explored the clinical value, function, and possible mechanism of miR-33a-5p in EC. We uncovered that miR-33a-5p and DKK1 are involved in the progression of EC. Significantly, the expression levels of miR-33a-5p were reduced and DKK1 levels were elevated in serum and tissues of clinical EC samples and in EC cell lines. The downregulation of miR-33a-5p and DKK1 upregulation were related to high TNM staging and poor differentiation of patients. The area under the curves (AUCs) of miR-33a-5p and DKK1 for the occurrence of EC were 0.914 and 0.900, respectively. Down-regulation of miR-33a-5p or overexpression of DKK1 indicated a worse prognosis. The miR-33a-5p overexpression or DKK1 depletion induced apoptosis and repressed proliferation, migration, and invasion of EC cells. The repression of miR-33a-5p by inhibitor or DKK1 overexpression presented the conversed effects on EC cells. Mechanically, miR-33a-5p suppressed DKK1 expression, and miR-33a-5p targeted DKK1 to affect the biological behavior of EC through the Wnt/β-catenin pathway. Meanwhile, miR-33a-5p inhibited the tumor growth of EC in vivo . Thus, we concluded that miR-33a-5p inhibited the progression of EC through the DKK1-mediated Wnt/β-catenin pathway. MiR-33a-5p and DKK1 can be used as potential therapeutic targets of EC.

No abstract