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Hao, J.

Publications and source records attributed to Hao, J..

At least 73 records · Page 4Linked to original sources

Structure determination of protein-peptide complexes from NMR chemical shift data using MELD.

Intrinsically disordered regions of proteins often mediate important protein-protein interactions. However, the folding upon binding nature of many polypeptide-protein interactions limits the ability of modeling tools to predict structures of such complexes. To address this problem, we have taken a tandem approach combining NMR chemical shift data and molecular simulations to determine structures of peptide-protein complexes. Here, we demonstrate this approach for polypeptide complexes formed with the extraterminal (ET) domain of bromo and extraterminal domain (BET) proteins, which exhibit a high degree of binding plasticity. This system is particularly challenging as the binding process includes allosteric changes across the ET receptor upon binding, and the polypeptide binding partners can form different conformations (e.g., helices and hairpins) in the complex. In a blind study, the new approach successfully modeled bound-state conformations and binding poses, using only backbone chemical shift data, in excellent agreement with experimentally-determined structures. The approach also predicts relative binding affinities of different peptides. This hybrid MELD-NMR approach provides a powerful new tool for structural analysis of protein-polypeptide complexes in the low NMR information content regime, which can be used successfully for flexible systems where one polypeptide binding partner folds upon complex formation.

biophysics↗

SerpinB3 drives cancer stem cell survival in glioblastoma

Despite therapeutic interventions for glioblastoma (GBM), cancer stem cells (CSCs) drive recurrence. The precise mechanisms underlying CSC therapeutic resistance, namely inhibition of cell death, are unclear. We built on previous observations that the high cell surface expression of junctional adhesion molecule-A drives CSC maintenance and identified downstream signaling networks, including the cysteine protease inhibitor SerpinB3. Using genetic depletion approaches, we found that SerpinB3 is necessary for CSC maintenance, survival, and tumor growth, as well as CSC pathway activation. The knockdown of SerpinB3 also increased apoptosis and susceptibility to radiation therapy. Mechanistically, SerpinB3 was essential to buffer cathepsin L-mediated cell death, which was enhanced with radiation. Finally, we found that SerpinB3 knockdown dramatically increased the efficacy of radiation in pre-clinical models. Taken together, our findings identify a novel GBM CSC-specific survival mechanism involving a previously uninvestigated cysteine protease inhibitor, SerpinB3, and provide a potential target to improve the efficacy of standard-of-care GBM therapies against therapeutically resistant CSCs. SummaryLauko et al. demonstrate a functional role for SerpinB3, which is elevated in glioblastoma cancer stem cells and protects against lysosomal-mediated cell death. SerpinB3 can be targeted to increase the efficacy of radiation in glioblastoma pre-clinical models.

cancer biology↗

A dual reporter system identifies an intermediate state and sequential regulators of 2-cell-like-to-pluripotent state transition

Mouse embryonic stem cells (ESCs) cycle in and out of 2-cell-like (2C-like) state in culture. The molecular mechanism governing the exit of 2C-like state remains obscure, partly due to the lack of a reporter system that can genetically mark intermediate states during exiting process. Here, we identify an intermediate state that is marked by the co-expression of MERVL::tdTomato and OCT4-GFP (MERLOT) during 2C-like-to-pluripotent state transition (2CLPT). Transcriptome and epigenome analyses demonstrate that MERLOT cells cluster closely with 8-16 cell stage mouse embryos, suggesting that 2CLPT partly mimics early preimplantation development. Through a CRISPRa screen, we identify an ARRDC3-NEDD4-OCT4 regulatory axis that plays an essential role in controlling 2CLPT. Furthermore, re-evaluating previously reported 2C-like state regulators reveals dual function of Chaf1a in regulating the entry and exit of 2C-like state. Finally, ATAC-Seq footprinting analysis uncovers Klf3 as an essential transcription factor required for efficient 2CLPT. Together, our study identifies a genetically traceable intermediate state during 2CLPT and provides a valuable tool to study molecular mechanisms regulating this process.

cell biology↗

Multiple ETS Factors Participate in the Transcriptional Control of TERT Mutant Promoter in Thyroid Cancers

Hotspot mutations in the TERT (telomerase reverse transcriptase) gene are key determinants of thyroid cancer progression. TERT promoter mutations (TPM) create de novo consensus binding sites for the ETS ("E26 transforming sequence") family of transcription factors. In this study, we systematically knocked down each of the 20 ETS factors expressed in thyroid tumors and screened their effects on TERT expression in seven thyroid cancer cell lines with defined TPM status. We observed that, unlike in other TPM-carrying cancers such as glioblastomas, ETS factor GABPA does not unambiguously regulate transcription from the TERT mutant promoter in thyroid specimens. In fact, multiple members of the ETS family impact TERT expression, and they typically do so in a mutation-independent manner. In addition, we observe that partial inhibition of MAPK, a central pathway in thyroid cancer transformation, is more effective at suppressing TERT transcription in the absence of TPMs. Taken together, our results show a more complex scenario of TERT regulation in thyroid cancers compared to other lineages, suggest that compensatory mechanisms by ETS and other regulators likely exist and advocate for the need of a more comprehensive understanding of the mechanisms of TERT deregulation in thyroid tumors before eventually exploring TPM-specific therapeutic strategies. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=157 HEIGHT=200 SRC="FIGDIR/small/472152v1_ufig1.gif" ALT="Figure 1"> View larger version (54K): org.highwire.dtl.DTLVardef@63d70corg.highwire.dtl.DTLVardef@bb5d3corg.highwire.dtl.DTLVardef@e613a5org.highwire.dtl.DTLVardef@113bf54_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Lateral plate mesoderm cell-based organoid system for NK cell regeneration from human pluripotent stem cells

Human pluripotent stem cell (hPSC)-induced NK (iNK) cells are a promising "off-the-shelf" cell product for universal immune therapy. Conventional methods for iNK cell regeneration from hPSCs include embryonic body-formation and feeder-based expansion steps, which bring instability, time-consuming, and high costs for manufacture. In this study, we develop an embryonic body-free, organoid aggregate method for NK cell regeneration from hPSCs. In a short time window of 27-day induction, millions of hPSC input can produce over billions of iNK cells without the necessity of NK cell-expansion feeders. The iNK cells highly express classical toxic granule proteins, apoptosis-inducing ligands, as well as abundant activating and inhibitory receptors. Functionally, the iNK cells eradicate human tumor cells by mechanisms of direct cytotoxity, apoptosis, and antibody-dependent cellular cytotoxicity. This study provides a reliable scale-up method for regenerating human NK cells from hPSCs, which promotes the universal availability of NK cell products for immune therapy.

immunology↗

scCODE: an R package for personalized differentially expressed gene detection on single-cell RNA-sequencing data

Differential expression (DE) gene detection in single-cell RNA-seq (scRNA-seq) data is a key step to understand the biological question investigated. We find that DE methods together with gene filtering have profound impact on DE gene identification, and different datasets will benefit from personalized DE gene detection strategies. Existing tools dont take gene filtering into consideration, and couldnt evaluate DE performance on real datasets without prior knowledge of true results. Based on two new metrics, we propose scCODE (single cell Consensus Optimization of Differentially Expressed gene detection), an R package to automatically optimize DE gene detection for each experimental scRNA-seq dataset.

bioinformatics↗

Developing a More Accurate Biomedical Literature Retrieval Method using Deep Learning and Citations in PubMed Central Full-text Articles

Most queries submitted to a literature search engine can be more precisely written as sentences to give the search engine more specific information. Sentence queries should be more effective, in principle, than short queries with small numbers of keywords. Querying with full sentences is also a key step in question-answering and citation recommendation systems. Despite the considerable progress in natural language processing (NLP) in recent years, using sentence queries on current search engines does not yield satisfactory results. In this study, we developed a deep learning-based method for sentence queries, called DeepSenSe, using citation data available in full-text articles obtained from PubMed Central (PMC). A large amount of labeled data was generated from millions of matched citing sentences and cited articles, making it possible to train quality predictive models using modern deep learning techniques. A two-stage approach was designed: in the first stage we used a modified BM25 algorithm to obtain the top 1000 relevant articles; the second stage involved re-ranking the relevant articles using DeepSenSe. We tested our method using a large number of sentences extracted from real scientific articles in PMC. Our method performed substantially better than PubMed and Google Scholar for sentence queries.

bioinformatics↗

Loss of TBK1 activity leads to TDP-43 proteinopathy through lysosomal dysfunction in human motor neurons

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by motor neuron loss accompanied by cytoplasmic localization of TDP-43 proteins and their insoluble accumulations. Haploinsufficiency of TBK1 has been found to associate with or cause ALS. However, the cell-autonomous mechanisms by which reduced TBK1 activity contributes to human motor neuron pathology remain elusive. Here, we generated a human cellular model harboring loss-of-function mutations of TBK1 by gene editing and found that TBK1 deficiency was sufficient to cause TDP-43 pathology in human motor neurons. In addition to its functions in autophagy, we found that TBK1 interacted with endosomes and was required for normal endosomal maturation and subsequent lysosomal acidification. Surprisingly, TDP-43 pathology resulted more from the dysfunctional endo-lysosomal pathway than the previously recognized autophagy inhibition mechanism. Restoring TBK1 levels ameliorated lysosomal dysfunction and TDP-43 pathology and maintained normal motor neuron homeostasis. Notably, using patient-derived motor neurons, we found that haploinsufficiency of TBK1 sensitized neurons to lysosomal stress, and chemical regulators of endosomal maturation rescued the neurodegenerative process. Together, our results revealed the mechanism of TBK1 in maintaining TDP-43 and motor neuron homeostasis and suggested that modulating endosomal maturation was able to rescue neurodegenerative disease phenotypes caused by TBK1 deficiency.

neuroscience↗

Decoding molecular and cellular heterogeneity of nucleus accumbens with high-throughput scRNA-seq and MERFISH

The nucleus accumbens (NAc) plays an important role in regulating multiple behaviors and its dysfunction has been linked to many neural disorders. However, the molecular, cellular and anatomic heterogeneity underlying its functional diversity remains incompletely understood. Here, we generate a cell census of the mouse NAc using high-throughput single cell RNA sequencing and multiplexed error-robust FISH, revealing a high level of cell heterogeneity in this brain region. We show that the transcriptional and spatial diversity of neuron subtypes underlie NAcs anatomic and functional heterogeneity, and possibly contribute to the pathogenesis of different neurological disorders. These findings explain how the seemingly simple neuronal composition of the NAc achieves its highly heterogenous structure and diverse functions. Collectively, our study generates a spatially resolved cell taxonomy for understanding the NAc structure and function, which demonstrates the importance of combining molecular and spatial information in revealing the fundamental features of the nervous system.

neuroscience↗

Single-cell RNA-sequencing reveals thoracolumbar vertebra heterogeneity and rib-genesis in pigs

Thoracolumbar vertebra (TLV) and rib primordium (RP) development is a common evolutionary feature across vertebrates although whole-organism analysis of TLV and RP gene expression dynamics has been lacking. Here we investigated the single-cell transcriptomic landscape of thoracic vertebra (TV), lumbar vertebra (LV), and RP cells from a pig embryo at 27 days post-fertilization (dpf) and identified six cell types with distinct gene-expression signatures. In-depth dissection of the gene-expression dynamics and RNA velocity revealed a coupled process of osteogenesis and angiogenesis during TLV and rib development. Further analysis of cell-type-specific and strand-specific expression uncovered the extremely high levels of HOXA10 3-UTR sequence specific to osteoblast of LV cells, which may function as anti-HOXA10-antisense by counteracting the HOXA10-antisense effect to determine TLV transition. Thus, this work provides a valuable resource for understanding embryonic osteogenesis and angiogenesis underlying vertebrate TLV and RP development at the cell-type-specific resolution, which serves as a comprehensive view on the transcriptional profile of animal embryo development.

developmental biology↗

A Novel Non-Invasive Epithelial Ovarian Cancer Mouse Model Of Hyperthermic Intraperitoneal Chemotherapy (HIPEC)

BackgroundHyperthermic intraperitoneal chemotherapy (HIPEC) in combination with interval cytoreductive surgery increases the overall survival of epithelial ovarian cancer (EOC) patients with advanced disease. Despite its proven benefits, the mechanism by which HIPEC extends overall survival remains unknown and current strategies to optimize HIPEC are therefore limited. A major challenge is the lack of a robust and streamlined model to investigate the mechanisms underlying HIPEC efficacy. ObjectiveTo introduce a novel murine model that can be used to enhance our understanding of HIPEC therapy. MethodID8-luc, an EOC mouse cell line, is inoculated into immunocompetent C57BL/6J mice intraperitoneally. Once tumor is detected by In Vivo Imaging System (IVIS), cisplatin (5 mg/kg) is injected intraperitoneally and superficial hyperthermia of 40{degrees}C is applied to the animals abdomen and pelvis using an FDA-approved hyperthermia unit (BSD500) for 20 minutes. To validate the model, four treatment conditions were tested: cisplatin and hyperthermia, cisplatin and normothermia, vehicle and hyperthermia, and vehicle and normothermia. Tumor growth was assessed over the course of treatment using IVIS optical spectrum. ResultsTumor growth in mice treated with hyperthermic cisplatin was significantly suppressed compared to mice treated with normothermic cisplatin (p < 0.05). No significant differences in tumor growth were observed in the hyperthermic vehicle and normothermic vehicle groups. ConclusionsWe developed an innovative noninvasive mouse model of HIPEC. Similar to patients with advanced ovarian cancer who are treated with HIPEC at the time of interval cytoreductive surgery, our model demonstrates that hyperthermia enhances the inhibitory effect of cisplatin on intraperitoneal tumor growth. Development of this murine model provides an opportunity to elucidate the mechanisms underlying HIPEC and offer an opportunity to test adjunct treatments in a pre-clinical setting to enhance the utility of HIPEC.

cancer biology↗

Discovery of novel ID2 antagonists from pharmacophore-based virtual screening as potential therapeutics for glioma

Glioma, especially the most aggressive type glioblastoma multiforme, is one of the central nervous system malignant cancer with a poor prognosis. Traditional treatments are mainly surgery combined with radiotherapy and chemotherapy, which is still not satisfactory. Therefore, it is of great clinical significance to find new therapeutic agents. Served as an inhibitor of differentiation, protein ID2 (inhibitor of DNA binding 2) plays an important role in neurogenesis, neovascularization and malignant development of gliomas. It has been shown that ID2 affects the malignant progression of gliomas through different mechanisms. In this study, a pharmacophore-based virtual screening was carried out and 16 hit compounds were purchased for pharmacological evaluations on their ID2 inhibitory activities. Based on the cytotoxicity of these small-molecule compounds, two compounds were shown to effectively inhibit the viability of glioma cells in the low micromolar range. Among them, AK-778-XXMU was chosen for further study due to its better solubility in water. A SPR assay proved the high affinity between AK-778-XXMU and ID2 protein with the KD value as 129 nM. The plausible binding mode in the biding site of ID2 was studied by molecular docking. Subsequently, the cancer-suppressing potency of the compound was characterized both in vitro and in vivo. The data demonstrated that compound AK-778-XXMU is a potent ID2 antagonist which has the potential to be developed as a therapeutic agent against glioma. HighlightsO_LITwo pharmacophores were built from the first-in-class pan-ID antagonists AGX51 C_LIO_LIA pharmacophore-based virtual screening was carried out and 16 hit compounds were purchased for pharmacological evaluations in glioma inhibition C_LIO_LICompound AK-778-XXMU was identified to be a potent ID2 antagonist in the low submicromolar range (KD: 159 nM) C_LI

cancer biology↗

A novel framework for single-cell Hi-C clustering based on graph-convolution-based imputation and two-phase-based feature extraction

The three-dimensional genome structure plays a key role in cellular function and gene regulation. Singlecell Hi-C technology can capture genome structure information at the cell level, which provides the opportunity to study how genome structure varies among different cell types. However, few methods are well designed for single-cell Hi-C clustering, because of high sparsity, noise and heterogeneity of single-cell Hi-C data. In this manuscript, we propose a novel framework, named ScHiC-Rep, for singlecell Hi-C data representation and clustering. ScHiC-Rep mainly contains two parts: data imputation and feature extraction. In the imputation part, a novel imputation workflow is proposed, including graph convolution-based, random walk with restart-based and genomic neighbor-based imputation. In the feature extraction part, a two-phase feature extraction method is proposed, including linear phase for chromosome level and non-linear phase for cell level feature extraction. The evaluation results show that the proposed framework outperforms existing state-of-the-art approaches on both human and mouse datasets.

bioinformatics↗

The Actin Bundling Protein Fascin Promotes Lung Cancer Growth and Metastasis by Enhancing Glycolysis and PFKFB3 Expression

Fascin is a pro-metastasis actin bundling protein upregulated in essentially all the metastatic carcinoma. It is believed that fascin promotes cancer cell migration and invasion by facilitating membrane protrusions such as filopodia and invadopodia. Aerobic glycolysis is a key feature of cancer metabolism that provides critical intermediate metabolites for tumor growth and cell proliferation. Here we report that fascin increase glycolysis in lung cancer to promote tumor growth and metastasis. Fascin promotes glycolytic flux by increasing the expression and activities of phosphofructose kinase 1 and 2 (PFK1 and 2). The glycolytic function of fascin depends on activation of YAP1 through its canonical actin bundling activity. Fascin promotes the binding of YAP1 to a TEAD1/4 binding motif located 30 bp upstream of the PFKFB3 transcription start site to activate its transcription. Our interrogation of the TCGA database suggest that the fascin-YAP1-PFKFB3 circuit is likely conserved across different types of cancer. We further showed that the glycolytic function of fascin is essential for promotion of lung cancer growth and metastasis. Importantly, pharmacological inhibitors of fascin could be used to suppress the YAP1-PFKFB3 signaling and inhibit glycolysis in cancer cell lines, organoid cultures and xenograft metastasis models. Taken together, our data reveal an important glycolytic role of fascin in lung cancer metabolism, and suggest that pharmacological inhibitors of fascin could be used to reprogram cancer metabolism in lung cancer and potentially other cancer with fascin upregulation.

cancer biology↗

Structure of SOQ1 lumenal domains identifies potential disulfide exchange for negative regulation of photoprotection, qH

Non-photochemical quenching (NPQ) plays an important role for phototrophs in decreasing photo-oxidative damage. qH is a sustained component of NPQ and depends on the plastid lipocalin (LCNP). A thylakoid membrane-anchored protein SUPPRESSOR OF QUENCHING1 (SOQ1) prevents qH formation by inhibiting LCNP. SOQ1 suppresses qH with its lumen-located C-terminal Trx-like and NHL domains. Here we report crystal structures and biochemical characterization of SOQ1 lumenal domains. Our results show that the Trx-like and NHL domains are stably associated, with the potential redox-active motif located at their interface. Residue E859 essential for SOQ1 function is pivotal for mediating the inter-domain interaction. Moreover, the C-terminal region of SOQ1 forms an independent {beta}-stranded domain, which possibly interacts with the Trx-like domain through disulfide exchange. Furthermore, SOQ1 is susceptible to cleavage at the loops connecting the neighboring domains both in vitro and in vivo, which could be a regulatory process for its suppression function of qH.

plant biology↗

Resolving the Interactions Between Class 3 Semaphorin Receptors in Live Cells

The plexin/neuropilin/semaphorin family of proteins is involved with tissue patterning in the developing embryo. These proteins play roles in cell migration and adhesion, but are also important in disease, including cancer angiogenesis and metastasis. While some structures of the soluble domains of these proteins have been determined, the conformations of full-length receptor complexes are just beginning to be studied, especially within the context of the cell plasma membrane. Pulsed-interleaved excitation fluorescence cross-correlation spectroscopy (PIE-FCCS) allows direct insight to the formation of protein-protein interactions in the membrane of live cells. Here we investigated the homodimerization of neuropilin-1, Plexin A2, Plexin A4, and Plexin D1. Consistent with previous studies, we found that neuropilin-1, Plexin A2 and Plexin A4 are dimers in the absence of exogenous ligand. Plexin D1, on the other hand, was monomeric under similar conditions, which had not been previously reported. We also found that Plexin A2 and A4 assemble into a heteromeric complex. Stimulation with Semaphorin 3A or Semaphorin 3C ligand neither disrupts nor enhances the dimerization of the receptors when they are expressed alone, suggesting that activation involves a conformational change rather than a shift in the monomer-dimer equilibrium. However, upon stimulation with Semaphorin 3C, Plexin D1 and neuropilin-1 form a heteromeric complex, while Semaphorin 3A does not induce a stable complex with these receptors. This analysis of interactions by PIE-FCCS provides a complementary approach to the existing structural and biochemical data that will aid in the development of new therapeutic strategies to target these receptors during disease.

biophysics↗

LPA/PKD-1 signaling promotes development of arteriolar niche that supports self-renewal of breast cancer stem cells and stemness

Breast cancer stem cells (BCSCs) are essential for cancer growth, metastasis and recurrence. However, the regulatory mechanisms of self-renewal and interactions with the vascular niche within tumor microenvironment are currently under investigation. Here, we demonstrate that BCSCs are enriched within arteriolar niche within the tumor microenvironment of estrogen receptor positive (ER+) BC and bi-directionally interact with arteriolar endothelial cells (ECs). Mechanistically, this interaction is driven by the LPA/PKD-1 signaling pathway, which promotes arteriolar differentiation and self-renewal. Furthermore, this pathway directly promotes stemness features. These findings suggest that targeting LPA/PKD-1 signaling may disrupt the arteriolar niche within the tumor microenvironment and concomitantly eradicate BCSCs, thereby attenuating BC progression.

cancer biology↗

A common binding motif in the ET domain of BRD3 forms polymorphic structural interfaces with host and viral proteins

The extra-terminal (ET) domain of BRD3 is conserved among BET proteins (BRD2, BRD3, BRD4), interacting with multiple host and viral protein-protein networks. Solution NMR structures of complexes formed between BRD3-ET domain with either the 79-residue murine leukemia virus integrase (IN) C-terminal domain (IN329-408), or its 22-residue IN tail peptide (TP) (IN386-407) alone, reveal similar intermolecular three-stranded {beta}-sheet formation. 15N relaxation studies reveal a 10-residue linker region (IN379-388) tethering the SH3 domain (IN329-378) to the ET-binding motif (IN389-405)-ET complex. This linker has restricted flexibility, impacting its potential range of orientations in the IN - nucleosome complex. The complex of the ET-binding peptide of host NSD3 protein (NSD3148-184) and BRD3-ET domain includes a similar three-stranded {beta}-sheet interaction, but the orientation of the {beta}-hairpin is flipped compared to the two IN : ET complexes. These studies expand our understanding of molecular recognition polymorphism in complexes of ET-binding motifs with viral and host proteins. HighlightsO_LIThe BRD3 ET domain binds to key peptide motifs of diverse host and viral proteins. C_LIO_LIThese complexes reveal conformational plasticity in molecular recognition. C_LIO_LINMR studies demonstrate restricted interdomain motion in the IN CTD / ET complex. C_LIO_LIA cost-effective approach is described for producing isotopically-labeled peptides. C_LI Etoc BlurbWe address structurally how the MLV Integrase (IN) usurps the host function of the BET protein through comparative studies of the IN : Brd3 ET complex with that of the host NSD3. MLV integration and thus its pathogenesis is driven through protein interactions of the IN : BET family.

microbiology↗