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Objectives: Oesophagectomy was always recommended after noncurative endoscopic resection (ER). And the optimal time interval from ER to oesophagectomy remains unclear. This study was to explore the effect of interval on pathologic stage and prognosis., Methods: We included 155 patients who underwent ER for cT1N0M0 oesophageal cancer and then received subsequent oesophagectomy from 2009 to 2019. Overall survival and disease-free survival (DFS) were analysed to find an optimal cut-off of interval from ER to oesophagectomy. In addition, pathologic stage after ER was compared to that of oesophagectomy. Logistic regression model was built to identify risk factors for pathological upstage., Results: The greatest difference of DFS was found in the groups who underwent oesophagectomy before and after 30 days (P = 0.016). Among total 155 patients, 106 (68.39%) received oesophagectomy within 30 days, while 49 (31.61%) had interval over 30 days. Comparing the pathologic stage between ER and oesophagectomy, 26 patients had upstage and thus had worse DFS (hazard ratio = 3.780, P = 0.042). T1b invasion, lymphovascular invasion and interval >30-day group had a higher upstage rate (P = 0.014, P < 0.001 and P < 0.001, respectively). And they were independent risk factors for pathologic upstage (odds ratio = 3.782, 4.522 and 2.844, respectively)., Conclusions: It was the first study exploring the relationship between time interval and prognosis in oesophageal cancer. The longer interval between noncurative ER and additional oesophagectomy was associated with a worse DFS, so oesophagectomy was recommended performed within 1 month after ER. Older age, T1b stage, lymphovascular invasion and interval >30 days were significantly associated with pathologic upstage, which is related to the worse outcome too., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Background: Marmesin, an important coumarin isolated from Broussonetia kazinoki, has been proposed to possess many pharmacological activities including anti-tumor activity. However, the anti-cancer effect of marmesin on esophageal cancer (EC) has not been characterized. The study aimed to explore the anti-cancer role of marmesin using EC cell lines in vitro., Methods and Results: Cell proliferation was evaluated by CCK-8 and Edu cell proliferation assays and apoptosis was detected by TUNEL assay. Western blot analysis was used to determine the expression of Ki67, proliferating cell nuclear antigen (PCNA), Bcl-2, Bax, phosphatidylinositol 3-kinase (PI3K), phosphoryrated-PI3K (p-PI3K), protein kinase B (Akt), and phosphoryrated-Akt (p-Akt). The mechanism of action of marmesin was analyzed using network pharmacology approach. Marmesin exhibited anti-proliferative effect against EC cells, which was further confirmed by the reduced expression of Ki67 and PCNA. Marmesin exerted pro-apoptotic activity on EC cells by downregulating Bcl-2 and upregulating Bax. According to the results from network pharmacology approach, we speculated that PI3K/Akt pathway may participate in the effect of marmesin on EC cells. Additionally, the PI3K/Akt pathway was suppressed by marmesin in EC cells. Moreover, forced expression of Akt reversed the inhibition of cell proliferation and induction of apoptosis induced by marmesin in EC cells., Conclusions: Marmesin exerted anti-cancer activity in EC cells by inhibiting the PI3K/Akt pathway., (© 2021. The Japan Esophageal Society.)

This study was aimed at investigating the effect of growth differentiation factor 11 (GDF11) on the proliferation and apoptosis of esophageal cancer cells. Serum levels of GDF11 in esophageal cancer patients were determined with ELISA kits, and the correlation between serum GDF11 and pathological features of esophageal cancer were determined. The effect of recombinant GDF11 on the growth of esophageal cancer cells was measured by CCK6 method. In order to investigate the effect of recombinant GDF11 on the proliferation and apoptosis of esophageal cancer cells, the expression of apoptosis-promoting protein Bax and proliferative-associated protein Bcl-2 in esophageal cancer cells were determined using western blot. Moreover, GDF11 was used to treat esophageal cancer cells, and its effect on proliferation and apoptosis was determined with MTT assay and flow cytometry, respectively. The serum content of GDF11 was much less in esophageal cancer patients than in the control group. Esophageal GDF II in cancer patients was correlated with cancer differentiation: the higher the degree of differentiation, the higher the content of GDF11. GDF11 inhibits proliferation and apoptosis of esophageal cancer cells.

KLK13 downregulation occurs in tumour tissues in comparison with adjacent normal tissues from patients with oesophageal squamous cell carcinoma (OSCC). KLK13 mRNA levels were tested in OSCC tumour tissues and adjacent noncancerous tissues from 138 patients. In addition, the correlation between KLK13 mRNA levels and OSCC clinicopathologic features was analysed. KLK13 mRNA levels decreased notably in tumour tissues compared with those in adjacent noncancerous tissues. And decreased KLK13 mRNA levels indicated significant correlations with higher tumour grade, elevated TNM (UICC, 2009) stage classification, deeper infiltration and more lymph node metastases. And thus KLK13 may be a promising diagnostic marker. Decreased KLK13 mRNA levels also correlate with poor survival, which indicates that KLK13 mRNA expression may be a potential prognostic marker, although it could not be an independent prognostic factor by multivariate analysis. In vitro experiments of the OSCC cell lines KYSE150 and KYSE450 demonstrated that overexpression of KLK13 inhibits cell invasion and migration. Thus, KLK13 is a unique novel molecule useful for monitoring OSCC progression. Full elucidation of the role of KLK13 in OSCC may reveal avenues for investigating the molecule's functional potential as a novel therapeutic drug for targeting OSCC., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Background/aims: Esophageal carcinoma is one of the most aggressive human cancers, and novel treatment modality is required. Although expressing adequate levels of functional tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors DR4/DR5, significant proportion of esophageal cancer cells exhibit resistance to the cytotoxic effect of this ligand. Licochalcone-A (LA), a flavonoid present in a variety of edible plants, exhibits a wide spectrum of pharmacologic properties such as anticancer, antioxidant, and anti-inflammatory activities., Methodology: Eca109 and TE1 cells were cultured and transfected, then their viability was detected using MTT assay. Immunoprecipitation and immunoblotting analysis and RT-PCR analysis were also performed., Results: In this study, we found that LA synergistically caused the TRAIL-induced apoptosis in Eca109 and TE1 cells. Such potentiation was achieved through inhibiting Akt activation and promoting proteasomal degradation of X-linked Inhibitor of Apoptosis Protein (XIAP) which mediated the survival signals and allow the cells to escape from apoptosis in various human cancers., Conclusions: The combination of TRAIL and LA might be a novel therapeutic strategy for esophageal carcinoma patients who fail to respond to standard chemotherapy.

Background: The molecular backgrounds that determine therapeutic effectiveness in esophageal cancer remain largely unknown. Breast cancer susceptibility gene 1 (BRCA1) expression has been found to switch the response to cisplatin- or paclitaxel-based chemotherapy. It remains unclear how variations in BRCA1 expression influence clinical outcomes in esophageal cancer., Patients and Methods: Quantitative real-time polymerase chain reaction (qPCR) was performed to examine BRCA1 mRNA expressions in paraffin-embedded specimens from 144 patients with advanced or metastatic esophageal squamous cell carcinoma who received cisplatin- or docetaxel-based first-line treatments., Results: Low BRCA1 mRNA expression correlated with increased response rate (RR; P = 0.025 and 0.017, respectively) and median overall survival (mOS; P = 0.002 and P<0.001, respectively) in cisplatin-based chemotherapy or chemoradiotherapy group and also correlated with decreased RR (P = 0.017 and 0.024, respectively) and mOS (both P<0.001) in docetaxel-based chemotherapy or chemoradiotherapy group. Multivariate analysis revealed that low BRCA1 expression was an independent prognostic factor in cisplatin-based chemotherapy (HR 0.29; 95%CI 0.12-0.71; P = 0.007) or chemoradiotherapy (HR 0.12; 95%CI 0.04-0.37; P<0.001) group and higher risk for mortality in docetaxel-based chemotherapy (HR 5.02; 95%CI 2.05-12.28; P<0.001) or chemoradiotherapy (HR 7.02; 95%CI 2.37-27.77; P<0.001) group., Conclusions: BRCA1 mRNA expression could be used as a predictive and prognostic marker in esophageal cancer who underwent first-line cisplatin- or docetaxel-based treatments.