BackgroundDysregulation of microRNAs (miRNAs) have been demonstrated to contribute to carcinogenesis. MiR-143-3p has been identified to function as a tumor suppressor in several tumors, but the role of miR-143-3p in esophageal squamous cell carcinoma (ESCC) has not been intensively investigated. Our aim was to evaluate the potential role of miR-143-3p in the progression of ESCC.MethodsThe expression levels of miR-143-3p and QKI-5 protein were measured in 80 resected ESCC tumor specimens and the clinicopathological significance of these levels determined. We also investigated the role of miR-143-3p in the regulation of QKI-5 expression in ESCC cell lines both in vivo and in vitro.ResultsMiR-143-3p levels were decreased in ESCC clinical samples and low expression of miR-143-3p was significantly associated with poor prognosis in ESCC patients. Ectopic expression of miR-143-3p suppressed proliferation and induced apoptosis in ESCC cells both in vivo and in vitro. Ectopic expression of miR-143-3p also reduced the metastatic potential of cells by selectively regulating epithelial–mesenchymal transition regulatory proteins. Furthermore, QKI-5 isoform was upregulated in ESCC tissues and was a direct target of miR-143-3p. Lastly, re-introduction of QKI-5 expression abrogated the inhibitory effects of miR-143-3p on ESCC cell proliferation and motility.ConclusionsOur results demonstrate that miR-143-3p acts as a tumor-suppressor by targeting QKI-5 in ESCC, suggesting that miR-143-3p is a potential therapy for the treatment of ESCC.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-016-0533-3) contains supplementary material, which is available to authorized users.

Cancer-associated fibroblasts (CAF) are recognized as one of the key determinants in the malignant progression of lung adenocarcinoma. And its contributions to chemoresistance acquisition of lung cancer has raised more and more attention. In our study, cancer associated fibroblasts treated with cisplatin conferred chemoresistance to lung cancer cells. Meanwhile, Interleukin-11(IL-11) was significantly up-regulated in the CAF stimulated by cisplatin. As confirmed in lung adenocarcinoma cells in vivo and in vitro, IL-11 could protect cancer cells from cisplatin-induced apoptosis and thus promote their chemoresistance. Furthermore, it was also observed that IL-11 induced STAT3 phosphorylation and increased anti-apoptotic protein Bcl-2 and Survivin expression in cancer cells. The effect could be abrogated by suppressing STAT3 phosphorylation or silencing IL-11Rα expression in cancer cells. In conclusion, chemotherapy-induced IL-11 upregulation in CAF promotes lung adenocarcinoma cell chemoresistance by activating IL-11R/STAT3 anti-apoptotic signaling pathway.

Esophageal squamous cell carcinoma (ESCC) is the most common histological type in China. MicroRNAs are endogenously expressed in mammals and play a significant role in tumor invasion and metastasis by targeting potential downstream genes. In the present study, microarray analysis showed that miR-375 expression was distinctly downregulated in ESCC compared with that in normal esophageal epithelium tissues. Then, luciferase reporter assay showed that SHOX2 was the direct downstream target of miR-375 and this interaction was confirmed by the rescue experiments. Quantitative polymerase chain reaction results also showed that SHOX2 expression was upregulated in ESCC cells and tissues. Further analysis showed that SHOX2 induced proliferation, invasion, and metastasis of ESCC both in vivo and in vitro. Moreover, the interaction between miR-375 and SHOX2 affected the epithelial-to-mesenchymal transition. We conclude that miR-375 may suppress invasion and metastasis of ESCC by directly targeting SHOX2. The miR-375/SHOX2 axis may be a novel therapeutic target for ESCC.

Esophageal squamous cell carcinoma (ESCC) is among the most aggressive malignancies and has a high incidence in China. MicroRNAs (miRNAs) are small endogenous RNAs that regulate multiple tumorigenic processes, including proliferation, invasion, metastasis and prognosis. Using miRNA expression profiling analysis, we found that miR-630 was markedly down-regulated in three ESCC tissue samples compared with that in paired normal esophageal tissues. Differential miR-630 expression was subsequently confirmed using quantitative real-time PCR. To determine whether miR-630 down-regulation could be considered as a diagnostic indicator and adverse prognostic factor, we investigated the association between miR-630 and clinicopathological characteristics in patients with ESCC. It was found that decreased miR-630 expression was associated with poor overall survival in these patients. In addition, we also explored the biological function of miR-630 by targeting Slug and investigated the correlation between miR-630 expression and epithelial-mesenchymal transition (EMT) progression in vivo and in vitro. Ectopic miR-630 expression could inhibit proliferation, invasion and metastasis, whereas miR-630 knockdown induced proliferation, invasion, metastasis and EMT traits. Overall, our study supports a role for miR-630 as a critical novel modulator in ESCC.

EPS may induce DCS cells to exhibit mature characteristics, and the mechanism involved is probably related to the inhibition of the JAK2/STAT3 signal pathway and promotion of the NF-κB signal pathway.

Sirtuin-1 (SIRT1), one member of the mammalian sirtuin family, has been suggested to play an essential role in the development and progression of many tumors. However, the relationship between expression of SIRT1 and prognosis of esophageal cancer is still unknown. This study aimed to investigate SIRT1 expression and its possible prognostic value in esophageal squamous cell carcinoma (ESCC). A total of 86 patients with ESCC were enrolled in our study group. Clinical data and matched tissues were collected. Western blotting and real-time quantitative reverse transcription PCR (RT-PCR) were carried out to explore the expression of SIRT1 in four human ESCC cell lines, one human normal epithelial cell line, and clinical ESCC tissues. Expression levels of SIRT1 protein in tissues of specimens were detected by immunohistochemistry (IHC). Survival analysis was carried out using the Kaplan-Meier method. Univariate and multivariate Cox regression analyses were performed to evaluate the correlation of SIRT1 expression with clinical features and prognosis of ESCC patients. Basal expression levels of SIRT1 protein in ESCC tumor tissues and cell lines were higher than those in the control groups. IHC analysis showed that expression levels of SIRT1 protein significantly correlated with TNM stage and lymph node status of ESCC patients. Moreover, upregulated SIRT1 expression was associated with poor clinical prognosis. High SIRT1 expression in ESCC could serve as an independent predictive biomarker for diagnosis and prognosis in ESCC patients.

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12943-016-0533-3.