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Bing Dong,1 Yang Yang,1,2Anna Han,1 Songnan Zhang,3 Zhenhua Lin,1,2Yixuan Wang,1 Junjie Piao1,21Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji 133002, People’s Republic of China; 2Key Laboratory of the Science and Technology Department of Jilin Province, Yanji 133002, People’s Republic of China; 3Department of Oncology, Affiliated Hospital of Yanbian University, Yanji 13302, People’s Republic of ChinaPurpose: Human hydroxysteroid dehydrogenase-like 2 (HSDL2) is a characterized SDR gene that not only catalyses the oxidation and reduction of multiple substrates but also regulates different metabolic and signalling pathways. Accumulating evidences suggest that HSDL2 play an important role in cancer progression. However, the role of HSDL2 in breast cancer has not yet been determined. Thus, this study aims to explore the relevance of HSDL2 in breast cancer progression.Patients and methods: The location of HSDL2 protein was detected in MDA-MB-231 breast cancer cells by using immunofluorescence (IF) staining. The expression level of HSDL2 was evaluated by immunohistochemical (IHC) staining in 119 breast cancer tissues and 40 normal breast tissues. Then, the correlations between the overexpression of HSDL2 and clinicopathological features of breast cancer patients were evaluated by using the chi-square test, and the survival rates were calculated by the Kaplan-Meier method. In addition, the role of HSDL2 in breast cancer proliferation was assessed by MTT and colony formation assays, and cell cycle distribution was detected by flow cytometry analysis and Western blot.Results: IF staining and IHC analysis consistently showed that HSDL2 was predominantly expressed in the cytoplasm of breast cancer cells. The positive rate of HSDL2 protein was significantly higher in breast cancer tissues (87.4%, 104/119) than in adjacent normal breast tissues (25%, 10/40) (p

Qianrong Wang,1,* Anna Han,1,* Liyan Chen,1,2 Jie Sun,1 Zhenhua Lin,1,2 Xianglan Zhang,3,4 Xiangshan Ren1,21Department of Pathology and Cancer Research Center, Yanbian University Medical College, Yanji 133002, People’s Republic of China; 2Key Laboratory of the Science and Technology Department of Jilin Province, Yanji 133002, People’s Republic of China; 3Department of Pathology, Yanbian University Hospital, Yanji City, Jilin Province, People’s Republic of China; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, KoreaCorrespondence: Xiangshan RenDepartment of Pathology & Cancer Research Center, Yanbian University Medical College, No. 977, Gongyuan Road, Yanji City 133002, People’s Republic of ChinaEmail renxsh@ybu.edu.cn*These authors contributed equally to this workBackground: Gastric cancer (GC) is a major leading cause of cancer mortality worldwide. Polyadenylate (poly(A))-binding protein (PABP)-interacting protein 1 (Paip1) is a key regulator in the initiation of translation; however, its role in GC remains to be investigated.Purpose: The purpose of this study is to determine Paip1 expression levels and investigate its underlying molecular mechanism in GC.Patients and methods: In the present study, a total of 90 GC samples and 90 adjacent noncancerous tissues were used to examine the expression of Paip1. In order to gain a deep insight into the molecular mechanism of Paip1 in GC, the Paip1 siRNA sequences were transfected into GC cell lines (MGC-803 and SGC-7901), respectively. Meanwhile, Paip1 plasmid was used to mediate overexpression of Paip1. Cell proliferation were examined via colony formation assay, EdU assay and flow cytometry assay. Cell metastasis were discovered via wound healing assay and Transwell assays. In addition, key EMT makers were detected by Western blotting assay.Results: In this study, Paip1 expression was observed to be upregulated in GC and was associated with shorter overall survival. Knockdown of Paip1 inhibited cell proliferation, migration and caused cell cycle arrest in GC cells, whereas its overexpression reversed these effects. Another mechanistic study showed that Paip1 overexpression promoted EMT progression and regulated its targets expression.Conclusion: High expression of Paip1 plays a significant role in the progression of GC and may be a potential biomarker of poor prognosis as well as a therapeutic target.Keywords: Paip1, metastasis, proliferation, gastric cancer, prognostic marker

© 2016 The Authors. Published by Oxford University Press on behalf of the Royal Astronomical Society. We present the data release paper for the Galaxy Zoo: Hubble (GZH) project. This is the third phase in a large effort to measure reliable, detailed morphologies of galaxies by using crowdsourced visual classifications of colour-composite images. Images in GZH were selected from various publicly released Hubble Space Telescope legacy programmes conducted with the Advanced Camera for Surveys, with filters that probe the rest-frame optical emission from galaxies out to z ~ 1. The bulk of the sample is selected to have mI814W < 23.5, but goes as faint as mI814W < 26.8 for deep images combined over five epochs. The median redshift of the combined samples is 〈 z 〉 = 0.9 ± 0.6, with a tail extending out to z ≃ 4. The GZH morphological data include measurements of both bulge- and disc-dominated galaxies, details on spiral disc structure that relate to the Hubble type, bar identification, and numerous measurements of clump identification and geometry. This paper also describes a new method for calibrating morphologies for galaxies of different luminosities and at different redshifts by using artificially redshifted galaxy images as a baseline. The GZH catalogue contains both raw and calibrated morphological vote fractions for 119 849 galaxies, providing the largest data set to date suitable for large-scale studies of galaxy evolution out to z ~ 1.

Figure S1. Effect of Zyflamend on the proliferation of a castrate resistant prostate cancer cells in vitro. CWR22Rv1 cells were treated with Zyflamend (0–200 μg/ml) from 0 to 96 h and cell proliferation was monitored using the MTT assay. (PDF 71 kb)

Figure S1. Effect of Zyflamend on the proliferation of a castrate resistant prostate cancer cells in vitro. CWR22Rv1 cells were treated with Zyflamend (0–200 μg/ml) from 0 to 96 h and cell proliferation was monitored using the MTT assay. (PDF 71 kb)

Figure S2. Effect of Zyflamend on the proliferation of a colorectal cancer cell line in vitro and the subsequent phosphorylation of AMPKα at Thr172. (A) HCT116 cells were treated with Zyflamend (0–200 μg/ml) from 0 to 72 h and cell proliferation was monitored using the MTT assay. (B) Phosphorylation of AMPKα at Thr172 was determined following Zyflamend treatment (200 μg/ml for 3 h). (PDF 254 kb)

Figure S2. Effect of Zyflamend on the proliferation of a colorectal cancer cell line in vitro and the subsequent phosphorylation of AMPKα at Thr172. (A) HCT116 cells were treated with Zyflamend (0–200 μg/ml) from 0 to 72 h and cell proliferation was monitored using the MTT assay. (B) Phosphorylation of AMPKα at Thr172 was determined following Zyflamend treatment (200 μg/ml for 3 h). (PDF 254 kb)