BackgroundProducts of the SOX gene family play important roles in the life process. One of the members, SOX7, is associated with the development of a variety of cancers as a tumor suppression factor, but its relevance with ovarian cancer was unclear. In this study, we investigated the involvement of SOX7 in the progression and prognosis of epithelial ovarian cancer (EOC) and the involved mechanisms.MethodsExpression profiles in two independent microarray data sets were analyzed for SOX7 between malignant and normal tissues. The expression levels of SOX7 in EOC, borderline ovarian tumors and normal ovarian tissues were measured by immunohistochemistry. We also measured levels of COX2 and cyclin-D1 to examine their possible involvement in the same signal transduction pathway as SOX7.ResultsThe expression of SOX7 was significantly reduced in ovarian cancer tissues compared with normal controls, strongly indicating that SOX7 might be a negative regulator in the Wnt/β-catenin pathway in ovarian cancer. By immunohistochemistry staining, the protein expression of SOX7 showed a consistent trend with that of the gene expression microarray analysis. By contrast, the protein expression level of COX2 and cyclin-D1 increased as the tumor malignancy progressed, suggesting that SOX7 may function through the Wnt/β-catenin signaling pathway as a tumor suppressor. In comparison between the protein expression levels of SOX7 with pathological features of the cancer, we found that SOX7 was down-regulated mainly in serous cystadenocarcinoma and advanced stages of the cancers.ConclusionsThe expression of SOX7 correlates with tumor progression as a tumor suppressor, possibly through the Wnt/β-catenin signaling pathway in ovarian cancers, suggesting that SOX7 may be a promising prognostic marker.Electronic supplementary materialThe online version of this article (doi:10.1186/s13048-014-0087-1) contains supplementary material, which is available to authorized users.

Acanthopanax senticosus (previously classified as Eleutherococcus senticosus), commonly known as Ciwujia or Siberian Ginseng, is a traditional Chinese medicine (TCM), widely used for its high medicinal value, such as antifatigue, anti-inflammation, antistress, anti-ulcer and cardiovascular functions, in China, Korea, Japan and Russia. In the past decades, researchers worldwide have conducted systematic investigations on this herb, from chemistry to pharmacology, and a large number of chemical components have been characterized for their significant pharmacological effects. However, reports about the anticancer effects of this plant had been rare until recently, when considerable pharmacological experiments both in vitro and in vivo were conducted to study the anticancer effects of this herb. A. senticosus has been found to have inhibitory effects on malignant tumors, such as those in the lung and liver, suggesting that A. senticosus has potential to be developed as an effective anticancer drug. This paper reviews recent findings on the pharmacological properties of A. senticosus, with a focus on its anticancer effects.

SOX7 as a tumor suppressor belongs to the SOX F gene subfamily and is associated with a variety of human cancers, including breast cancer, but the mechanisms involved are largely unclear. In the current study, we investigated the interactions between SOX7 and AXIN2 in their co-regulation on the Wnt/β-catenin signal pathway, using clinical specimens and microarray gene expression data from the GEO database, for their roles in breast cancer. We compared the expression levels of SOX7 and other co-expressed genes in the Wnt/β-catenin pathway and found that the expression of SOX7, SOX17 and SOX18 was all reduced significantly in the breast cancer tissues compared to normal controls. AXIN2 had the highest co-relativity with SOX7 in the Wnt/β-catenin signaling pathway. Clinicopathological analysis demonstrated that the down-regulated SOX7 was significantly correlated with advanced stages and poorly differentiated breast cancers. Consistent with bioinformatics predictions, SOX7 was correlated positively with AXIN2 and negatively with β-catenin, suggesting that SOX7 and AXIN2 might play important roles as co-regulators through the Wnt-β-catenin pathway in the breast tissue to affect the carcinogenesis process. Our results also showed Smad7 as the target of SOX7 and AXIN2 in controlling breast cancer progression through the Wnt/β-catenin signaling pathway.Breast cancer is the most common malignant tumor in female and among the leading cancer deaths worldwide, with the incidence rapidly increasing in both American and Asian countries 1,2 . Breast cancer classification and stage evaluation have traditionally been based on clinicopathological features (patient age, lymph node invasion, tumor size, histological type, and pathology grade) 3 , but recent technological advances have made it possible to differentiate breast cancers by molecular markers such as ER (Estrogen Receptor), PR (Progesterone Receptor) and HER2 (Human epidermalgrowth factor receptor-2) 4,5 . Among the high risk genetic factors hitherto known to contribute to the pathogenesis of breast cancer are BRCA1 (Breast Cancer Type 1 Susceptibility Protein), BRCA2 (Breast Cancer Type 2 Susceptibility Protein) and TP53 (Tumor protein p53), which have high penetrance for the disease 6 . Over the past decade, extensive research has been focused on the identification of cellular signaling pathways involved in breast cancer, such as MAPK (Mitogen-activated protein kinases), PI3K/ Akt (Phosphatidylinositol-3-kinase/Akt) and Wnt/β -catenin signal pathways 7-10 . However, it still seems far away from a full picture of the molecular mechanisms underlying the breast carcinogenesis, which may involve a much greater variety of pathways and factors to be identified.

Background: Gastrointestinal acute radiation injury syndrome (GI-ARS) is potentially lethal and may occur after exposure to high radiation doses. Various chemical and biological agents have been developed to treat GI-ARS. However, their clinical utility is limited as they induce serious adverse reactions at their effective doses. Chinese herbal medicines have attracted attention because of their protective efficacy and low toxicity in radiation exposure treatment. However, their cellular and molecular mechanisms remain unknown. Here, we investigated the effects of the Chinese herbal Liangxue-Guyuan-Yishen decoction (LXGYD) on the intestinal stem cells and signal pathways of a GI-ARS rat model. Currently, there are limited treatment methods available globally; LXGYD might be a potential therapeutic option for patients with GI-ARS. Methods: The rat GI-ARS model was prepared by whole-body irradiation with 10-Gy of 60Co-γ rays. Various LXGYD concentrations were intragastrically administered to the irradiated rats. Health status and survival of the rats were evaluated and the protective efficacy of LXGYD on the intestines was assayed by pathological analysis. The active principles in LXGYD were detected by liquid chromatography-mass spectrometry (LC-MS) and their potential targets and pathways were screened by network pharmacological analysis. Intestinal stem cell proliferation, intestinal epithelial tight junction (TJ) protein expression, and regulatory pathways were explored by immunohistochemistry (IHC), western blotting (WB), and real-time quantitative polymerase chain reaction (RT-qPCR), respectively.Results: LXGYD administration significantly improved health status and survival in GI-ARS rats. The pathological analysis showed that LXGYD ameliorated radiation-induced intestinal injury. The LXGYD infusion significantly promoted LGR5+ stem cell regeneration in the ileal crypts, upregulated TJ proteins, and accelerated crypt reconstruction in the irradiated rats in a dose-dependent manner. LC-MS revealed ≥ 13 LXGYD constituents that might contribute to its protective effects. Involvement of the WNT and MEK/ERK pathways in intestinal repair and recovery were screened by network pharmacology analysis and validated by western blotting.Conclusions: The present study disclosed a heretofore unrecognized role of the Chinese herbal LXGYD in rescuing the intestinal stem cells of a GI-ARS rat model. It also showed that the WNT and MEK/ERK pathways may be involved in LXGYD-mediated intestinal regeneration in GI-ARS.