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Dive into the research topics where Shaohua Yao is active.

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Featured researches published by Shaohua Yao.


PLOS ONE | 2014

A PCR Based Protocol for Detecting Indel Mutations Induced by TALENs and CRISPR/Cas9 in Zebrafish

Chuan Yu; Yaguang Zhang; Shaohua Yao; Yuquan Wei

Genome editing techniques such as the zinc-finger nucleases (ZFNs), transcription activator-like effecter nucleases (TALENs) and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (Cas) system Cas9 can induce efficient DNA double strand breaks (DSBs) at the target genomic sequence and result in indel mutations by the error-prone non-homologous end joining (NHEJ) DNA repair system. Several methods including sequence specific endonuclease assay, T7E1 assay and high resolution melting curve assay (HRM) etc have been developed to detect the efficiency of the induced mutations. However, these assays have some limitations in that they either require specific sequences in the target sites or are unable to generate sequencing-ready mutant DNA fragments or unable to distinguish induced mutations from natural nucleotide polymorphism. Here, we developed a simple PCR-based protocol for detecting indel mutations induced by TALEN and Cas9 in zebrafish. We designed 2 pairs of primers for each target locus, with one putative amplicon extending beyond the putative indel site and the other overlapping it. With these primers, we performed a qPCR assay to efficiently detect the frequencies of newly induced mutations, which was accompanied with a T-vector-based colony analysis to generate single-copy mutant fragment clones for subsequent DNA sequencing. Thus, our work has provided a very simple, efficient and fast assay for detecting induced mutations, which we anticipate will be widely used in the area of genome editing.


Cancer Research | 2017

Long non-coding RNA LINC00092 acts in cancer-associated fibroblasts to drive glycolysis and progression of ovarian cancer

Linjie Zhao; Gaili Ji; Xiaobing Le; Chenlu Wang; Lian Xu; Min Feng; Yaguang Zhang; Huiliang Yang; Yu Xuan; Yanfei Yang; Lingzi Lei; Qilian Yang; Wayne Bond Lau; Bonnie Lau; Yi Chen; Xiangbing Deng; Shaohua Yao; Tao Yi; Xia Zhao; Yuquan Wei; Shengtao Zhou

The majority of patients with epithelial ovarian cancer are diagnosed at a late stage when the peritoneal metastases exist; however, there is little knowledge of the metastatic process in this disease setting. In this study, we report the identification of the long noncoding RNA LINC00092 as a nodal driver of metastatic progression mediated by cancer-associated fibroblasts (CAF). Prometastatic properties of CAFs in vitro and in vivo were found to associate with elevated expression of the chemokine CXCL14. In clinical specimens, elevated levels of CXCL14 in CAFs also correlated with poor prognosis. Notably, CXCL14-high CAFs mediated upregulation of LINC00092 in ovarian cancer cells, the levels of which also correlated with poor prognosis in patients. Mechanistic studies showed that LINC00092 bound a glycolytic enzyme, the fructose-2,6-biphosphatase PFKFB2, thereby promoting metastasis by altering glycolysis and sustaining the local supportive function of CAFs. Overall, our study uncovered a positive feedback loop in the metabolism of CXCL14-positive CAFs and ovarian cancer cells that is critical for metastatic progression. Cancer Res; 77(6); 1369-82. ©2017 AACR.


Biochimie | 2009

A novel pro-apoptosis gene PNAS4 that induces apoptosis in A549 human lung adenocarcinoma cells and inhibits tumor growth in mice

Fei Yan; Lantu Gou; Jinliang Yang; Lijuan Chen; Aiping Tong; Minghai Tang; Zhu Yuan; Shaohua Yao; Peng Zhang; Yuquan Wei

The gene PNAS4 is a high conservative gene that shares high homology of sequence in various organisms from plants to animals. We found overexpression of human PNAS4 induced apoptosis and arrested cell cycle in S phase in A549 human lung adenocarcinoma cells. In C57BL/6 mice model of Lewis lung carcinoma, overexpression of mouse PNAS4 significantly suppressed tumor growth and prolonged survival time through induction of tumor cell apoptosis, exhibiting effective antitumor. Our original investigations in vitro and vivo indicated PNAS4 is a novel pro-apoptosis gene, which could be used as a potential target of cancer biotherapy in future.


Journal of Biological Chemistry | 2011

APOA-II DIRECTS MORPHOGENETIC MOVEMENTS OF ZEBRAFISH EMBRYO BY PREVENTING CHROMOSOME FUSION DURING NUCLEAR DIVISION IN YOLK SYNCYTIAL LAYER

Ting Zhang; Shaohua Yao; Ping Wang; Chaoran Yin; Chun Xiao; Meilin Qian; Donghui Liu; Lemin Zheng; Wentong Meng; Hongyan Zhu; Jin Liu; Hong Xu; Xianming Mo

The high density lipoprotein (HDL) represents a class of lipid- and protein-containing particles and consists of two major apolipoproteins apoA-I and apoA-II. ApoA-II has been shown to be involved in the pathogenesis of insulin resistance, adiposity, diabetes, and metabolic syndrome. In embryo, apoa2 mRNAs are abundant in the liver, brain, lung, placenta, and in fish yolk syncytial layer (YSL), suggesting that apoa2 may perform a function during embryonic development. Here we find out that apoa2 modulates zebrafish embryonic development by regulating the organization of YSL. Disruption of apoa2 function in zebrafish caused chromosome fusing, which strongly blocked YSL nuclear division, inducing disorders in YSL organization and finally disturbing the embryonic epiboly. Purified native human apoA-II was able specifically to rescue the defects and induced nuclear division in zebrafish embryos and in human HeLa cells. The C terminus of apoA-II was required for the proper chromosome separation during nuclear division of YSL in zebrafish embryos and in human HeLa cells. Our data indicate that organization of YSL is required for blastoderm patterning and morphogenesis and suggest that apolipoprotein apoA-II is a novel factor of nuclear division in YSL involved in the regulation of early zebrafish embryonic morphogenesis and in mammalian cells for proliferation.


FEBS Letters | 2008

Pnas4 is a novel regulator for convergence and extension during vertebrate gastrulation

Shaohua Yao; Lifang Xie; Meilin Qian; Hanshuo Yang; Lang Zhou; Qian Zhou; Fei Yan; Lantu Gou; Yuquan Wei; Xia Zhao; Xianming Mo

Recent studies show that human Pnas4 might be tumor associated, while its function remains unknown. Here, we investigate the developmental function of Pnas4 using zebrafish as a model system. Knocking down Pnas4 causes gastrulation defects with a shorter and broader axis, as well as a posteriorly mis‐positioned prechordal plate, due to the defective convergence and extension movement. Conversely, over‐expression of Pnas4 mRNA leads to an elongated body axis. We further demonstrate that Pnas4 is required cell‐autonomously for dorsal convergence but not for anterior migration. In addition, genetic interaction assays indicate that Pnas4 might act in parallel with non‐canonical Wnt signal in the regulation of cell movement. Our data suggest that Pnas4 is a key regulator of cell movement during gastrulation.


Journal of Biological Chemistry | 2010

Kzp controls canonical Wnt8 signaling to modulate dorsoventral patterning during zebrafish gastrulation.

Shaohua Yao; Meilin Qian; Senyi Deng; Lifang Xie; Hanshuo Yang; Chun Xiao; Ting Zhang; Hong Xu; Xia Zhao; Yuquan Wei; Xianming Mo

During vertebrate embryonic development, the body axis formation requires the action of Wnt signals and their antagonists. Zygotic canonical wnt8 expression appears exclusively at the ventrolateral margin and mediates Wnt/β-catenin activities to promote posterior and ventral cell fate. However, the mechanisms involved in the initiation of zygotic wnt8 signals are poorly understood. Here, we identify a novel, maternally derived transcription factor, Kzp (Kaiso zinc finger-containing protein), as an important determinant for the initiation of zygotic Wnt signals in zebrafish. Kzp is a DNA-binding transcription factor that recognizes specific consensus DNA sequences, 5′-(t/a/g)t(a/t/g)nctgcca-3′, through zinc fingers and controls the initiation of zygotic wnt8 expression by directly binding to the wnt8 promoter during zebrafish embryonic development. Depletion of Kzp strongly dorsalized embryos, which was characterized by the expansion of dorsal gene expression. Overexpression of Kzp caused posteriorization. These phenotypes were highly similar to ones induced by wnt8 depletion or overexpression and were rescued by alteration of wnt8 activity. Thus, our results provide the first insight into the mechanism involved in the initiation of zygotic canonical Wnt signals by a maternally derived transcription factor.


Journal of Biological Chemistry | 2014

The Translation Initiation Factor eIF3i Up-regulates Vascular Endothelial Growth Factor A, Accelerates Cell Proliferation, and Promotes Angiogenesis in Embryonic Development and Tumorigenesis

Yike Yuan; Yaguang Zhang; Shaohua Yao; Huashan Shi; Xi Huang; Yuhao Li; Yuquan Wei; Shuo Lin

Background: Hypoxia regulates VEGFA expression at both the transcriptional and post-transcriptional levels. Results: eIf3i is induced by HIF1A under hypoxia and controls VEGFA protein translation. Conclusion: eIF3i controls VEGFA signaling during normal and tumorigenic angiogenesis. Significance: Our data reveal a new mechanism for VEGFA regulation, and eIF3i can be an oncotarget in anticancer therapies. Vascular endothelial growth factor A (VEGFA) is a critical proangiogenic factor that is activated by hypoxia at both the transcriptional and post-transcriptional levels. In hypoxia conditions, stabilized hypoxia-inducible factor 1α (HIF1A) is the key regulator for transcriptional activation of VEGFA. However, the post-transcriptional control of VEGFA expression remains poorly understood. Here, we report that the eukaryotic translation initiation factor 3i (eIF3i) is required for VEGFA protein expression in both normal embryonic and tumorigenic angiogenesis. eIF3i is dynamically expressed in the early stages of zebrafish embryogenesis and in human hepatocellular carcinoma tissues. eIF3i homozygous mutant zebrafish embryos show severe angiogenesis defects and human hepatocellular cancer cells with depletion of eIF3i to induce less angiogenesis in tumor models. Under hypoxia, the HIF1A protein can interact with its binding sequence in the eIF3i promoter and activate eIF3i transcription. The expression of VEGFA, which should rise in hypoxia, is significantly inhibited by eIF3i siRNA treatment. Moreover, eIF3i knockdown did not cause a general translation repression but specifically reduced the translation efficiency of the VEGFA mRNAs. Taken together, our results suggest that eIF3i is induced by HIF1A under hypoxia and controls normal and tumorigenic angiogenesis through regulating VEGFA protein translation.


Journal of Immunology | 2014

Ammonia Drives Dendritic Cells into Dysfunction

Can Luo; Guobo Shen; Ning Liu; Fengming Gong; Xiawei Wei; Shaohua Yao; Dan Liu; Xiu Teng; Ning Ye; Nan Zhang; Xikun Zhou; Jiong Li; Li Yang; Xia Zhao; Rong Xiang; Yuquan Wei

Ammonia levels are often elevated in patients with cirrhosis or tumors. Patients with these diseases are immunocompromised. In this study, we investigated the effects of ammonia on a member of the immune cell family, the dendritic cells (DCs). Our results demonstrated that ammonia diminished cell count, phagocytosis, and lymphocyte stimulation of DCs. Ammonia also induced DC swelling, excessive reactive oxygen species production, and mitochondrial damage, which may constitute the underlying mechanism of ammonia-induced DC dysfunction. In ammonium chloride (NH4Cl)–loaded mice, DCs exhibited lowered phagocytosis and a weakened immune response to the chicken OVA vaccine. DCs from patients with cirrhosis or ammonia-treated healthy human blood both exhibited diminished phagocytosis. Moreover, tumor cell conditioned medium drove DCs into dysfunction, which could be reversed by ammonia elimination. In a murine colon carcinoma model, we found that ammonia could regulate tumor growth involving DCs and their related immune response. These findings reveal that ammonia could drive DCs into dysfunction, which contributes to the immunocompromised state of patients with cirrhosis or tumors.


Developmental Biology | 2013

ENC1-like integrates the retinoic acid/FGF signaling pathways to modulate ciliogenesis of Kupffer's Vesicle during zebrafish embryonic development.

Meilin Qian; Shaohua Yao; Lulu Jing; Jiao He; Chun Xiao; Ting Zhang; Wentong Meng; Hongyan Zhu; Hong Xu; Xianming Mo

The left-right asymmetry is an essential feature shared by vertebrates. Cilia-driven counterclockwise flow in the mammalian node structure leads to the left-right asymmetric distribution of signals and subsequent asymmetric patterning. Although several signaling pathways have been identified in the specification of node ciliated cells, little is known about the direct downstream effectors of these signaling pathways. Here, we showed that zebrafish Ectoderm-Neural Cortex1-like (enc1l) is expressed in the Kupffers Vesicle (KV), an equivalent structure of the mammalian node in zebrafish, and is necessary for KV ciliogenesis. Loss-of-function of enc1l increased the number and decreased the length of KV cilia. The enc1l expression in the KV region was specifically regulated by retinoic acid (RA), FGF, and Wnt signaling pathways. In addition, knocking down enc1l or ectopic enc1l expression was able to rescue the KV cilium defects caused by alteration of RA and FGF signaling, but not Wnt signaling. Taken together, these data indicate thatEnc1l is a direct downstream effector of RA and FGF signaling pathways and modulates KV ciliogenesis in the zebrafish embryo.


BioMed Research International | 2010

Identification, Characterization, and Effects of Xenopus laevis PNAS-4 Gene on Embryonic Development

Fei Yan; Xu-Zhi Ruan; Hanshuo Yang; Shaohua Yao; Xinyu Zhao; Lantu Gou; Fanxin Ma; Zhu Yuan; Hongxin Deng; Yuquan Wei

Apoptosis plays an important role in embryonic development. PNAS-4 has been demonstrated to induce apoptosis in several cancer cells. In this study, we cloned Xenopus laevis PNAS-4 (xPNAS-4), which is homologous to the human PNAS-4 gene. Bioinformatics analysis for PNAS-4 indicated that xPNAS-4 shared 87.6% identity with human PNAS-4 and 85.5% with mouse PNAS-4. The phylogenetic tree of PNAS-4 protein was also summarized. An analysis of cellular localization using an EGFP-fused protein demonstrated that xPNAS-4 was localized in the perinuclear region of the cytoplasm. RT-PCR analysis revealed that xPNAS-4, as a maternally expressed gene, was present in all stages of early embryo development. Whole-mount in situ hybridization showed that xPNAS-4 was mainly expressed in ectoderm and mesoderm. Furthermore, microinjection of xPNAS-4 mRNA in vivo caused developmental defects manifesting as a small eye phenotype in the Xenopous embryos, and as a small eye or one-eye phenotype in developing zebrafish embryos. In addition, embryos microinjected with xPNAS-4 antisense morpholino oligonucleotides (MOs) exhibited a failure of head development and shortened axis.

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Fei Yan

Chinese Academy of Sciences

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