Publications by authors named "Chunyang Xing"

Background: Osteosarcoma (OS) is one of the most common malignancies arising in bone. Hypoxia and immune regulation are pivotal in tumor biology. However, their combined effects and mechanisms in OS remain understudied.

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Propriospinal detour pathways facilitate motor recovery after spinal cord injury (SCI). Here, through a screen of epigenetic modulators, we demonstrated that small interfering RNA (siRNA)-mediated knockdown of histone deacetylase 3, delivered by extracellular vesicles (EVsiHDAC3), promoted neurite outgrowth in murine spinal neurons and human induced pluripotent stem cell-derived sensory and motor neurons. To enhance in vivo efficacy, we developed a neurotrophic nanoparticle platform using gelatin methacryloyl microspheres conjugated with an optimized rabies glycoprotein-derived peptide.

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Background: Osteosarcoma is one of the five leading causes of cancer death among all pediatric malignancies. Recent advances in non-coding RNAs suggested that many long noncoding RNAs (lncRNAs) are dysregulated in cancer tissues and play important roles in carcinogenesis. We aimed to further explore the mechanisms of Long Intergenic Non-Protein Coding RNA 313 (LINC00313)-promoted malignant phenotypes of osteosarcoma.

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Retraction of: 'Anticancer activity of Fisetin against the human osteosarcoma cell lines involves G2/M cell cycle arrest, mitochondrial apoptosis and inhibition of cell migration and invasion', by Chunyang Xing, Yuzhu Zhang, Rong Su, Ronghuan Wu JBUON 2019;25(2):1022-1027; PMID:32521901. Following the publication of the above article, readers drew to our attention that part of the data was unreliable. The authors were requested to provide the raw data to prove the originality, but were unable to do so.

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Glioma is a malignant primary brain tumor that occurs in the central nervous system and has threatened the well-being of millions of patients. It is well acknowledged that long non-coding RNA (lncRNA) SNHG3 participates in the regulation of proliferation, inflation, differentiation, and metastasis in many cancers. However, the regulatory effect of SNHG3 on glioma progression is still controversial.

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Purpose: Osteosarcoma is rare but fatal type of human malignancy. The high metastasis rate, late diagnosis, emergence of drug resistance against drugs such as doxorubicin, and the lack of therapeutic targets obstructs the treatment of osteosarcoma. The present investigation explores the anticancer properties of Fisetin against human osteosarcoma cells.

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In the publication of our publication [1], we have noticed there is a wrong label in Fig. 1e, in which the position of "HCC" and "Adjacent" should be transposed.

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Background: Plant homeodomain finger protein 8 (PHF8) serves an activator of epithelial-mesenchymal transition (EMT) and is implicated in various tumors. However, little is known about PHF8 roles in hepatocellular carcinoma (HCC) and regulating E-cadherin expression.

Methods: PHF8 expression pattern was investigated by informatic analysis and verified by RT-qPCR and immunochemistry in HCC tissues and cell lines.

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Chondrosarcomas are malignant tumors of the bone that exhibit resistance to chemotherapy and radiation. Pyrroloquinoline quinone (PQQ) is a bacterial redox co‑factor and antioxidant that has been found to induce apoptosis in various cancer cells. This study investigated the role of PQQ in cell apoptosis of chondrosarcoma cells and the underlying pathways involved.

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Breast cancer (BC) is the most common female malignancy within the spectrum of human cancer. One promising way to reduce the mortality and morbidity of BC is to explore novel diagnostic markers for early diagnosis and prognostication. The neutrophil lymphocyte ratio (NLR) is a good reflection of inflammation, which plays an important role in tumor progression and metastasis.

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Background: Increasing evidence indicates that downregulation of cell adhesion molecule 1 (CADM1) contributes to tumorigenesis in various cancers. The present study was undertaken to investigate the CADM1 expression pattern in human hepatocellular carcinoma (HCC), and to elucidate the mechanism underlying CADM1-mediated tumor suppression.

Methods: CADM1 expression in HCC cell lines was measured by quantitative real-time PCR.

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The decrease of microRNA-452 (miR-452) in gliomas promoted stem-like features and tumorigenesis. However, the role of miR-452, especially in regulating cancer stem cells (CSCs) in hepatocellular carcinoma (HCC) remains ambiguous. We enriched stem-like HCC cells by serial passages of hepatospheres with chemotherapeutic agents.

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Our previous study has demonstrated that RNF43 could regulate the cell cycle in a p53-dependent manner in HCC. In this study, we aimed to access whether RNF43 could interact with cell cycle proteins involved in p53 pathway, including pRB, Cyclin D1 and MDM2. Totally, 123 paired HCC tissues and corresponding noncancerous tissues from HCC patients were included, and the expression of Cyclin D1, pRB and MDM2 was analyzed using tissue microarray.

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Background: It has been found that microRNA-423-5p (miR423-5p) is an oncogenic factor and frequently upregulated in gastric carcinoma. However, the involvement of miR423-5p in hepatocellular carcinoma (HCC) has been rarely reported. The aim of this study was to assess whether miR423-5p is aberrantly expressed in HCC tissues, and to characterize its roles in the cancerous biology of HCC.

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Article Synopsis
  • - MRC-5 fibroblasts, a type of carcinoma-associated fibroblast (CAF), play a significant role in enhancing the migration and invasion of hepatocellular carcinoma (HCC) cells, particularly through a process called non-classical epithelial-mesenchymal transition (EMT).
  • - The study showed that MRC-5 conditioned medium (MRC-5-CM) triggered changes in cell adhesion proteins and increased activity in pathways involving integrins and MMP2, leading to greater motility and invasiveness in specific HCC cell lines (Bel-7402 and MHCC-LM3).
  • - Interestingly, MRC-5-CM had different effects on the cell cycle and apoptosis in the two H
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Hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers in China. It is important to understand the genetic mechanisms underlying the development and progression of HBV-related HCC and to identify new biomarkers for clinical treatment. The important role of fibroblast growth factor receptors (FGFRs) has been widely recognized in many types of cancers, but the association between FGFR polymorphisms and HCC carcinogenesis has been rarely reported.

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  • The study investigates the role of microRNA-200a (miR-200a) in hepatocellular carcinoma (HCC), finding it often downregulated in cancer cells.
  • Results suggest that lower levels of miR-200a are linked to poorer overall survival for HCC patients.
  • Laboratory tests demonstrate that miR-200a inhibits HCC cell growth by causing cell cycle arrest, with CDK6 identified as a key target, highlighting its potential as a tumor suppressor.
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Background: Increasing evidence indicates that deregulation of microRNAs (miRNAs) is involved in tumorigenesis. Downregulation of microRNA-503 has been observed in various types of diseases, including cancer. However, the biological function of miR-503 in hepatocellular carcinoma (HCC) is still largely unknown.

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Article Synopsis
  • * Researchers used two cell culture models to simulate direct and indirect interactions between HCC cells (Bel-7402) and different types of normal cells, measuring key protein expressions to understand the effects on cell behavior.
  • * Results revealed that direct co-culture with normal liver cells increased E-cadherin expression and reduced the invasive capabilities of HCC cells, while indirect culture in lung fibroblast medium induced a more aggressive EMT-like transformation, highlighting the complex
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The rapid growth of hepatocellular carcinoma (HCC) leading to tumor hypoxia is a common pathological phenomenon. Meanwhile, tumor hypoxia can promote a change in the biological properties of tumor cells. It may enhance the survival of tumor cells under stress conditions, resulting in resistance to apoptosis and angiogenesis.

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Article Synopsis
  • - RNF43 is frequently overexpressed in hepatocellular carcinoma (HCC) and its high levels are linked to aggressive tumor characteristics like vascular invasion and poor differentiation.
  • - Reducing RNF43 expression leads to apoptosis and hinders various cancer cell behaviors, like proliferation and invasion, indicating its role in HCC growth.
  • - The study identified 229 genes affected by RNF43 knockdown, many related to cancer development, suggesting targeting RNF43 could be a promising approach for HCC treatment.
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  • Cyclin-dependent kinase inhibitor 3 (CDKN3) is a protein that affects cell cycling and has been linked to various cancers, but its specific role in hepatocellular carcinoma (HCC) is not well understood.
  • Research showed that CDKN3 is often overexpressed in HCC cell lines and patient samples, correlating with less differentiated tumors and more advanced stages of cancer.
  • Further studies indicated that CDKN3 promotes cell growth during a specific phase of the cell cycle without affecting cell death or invasion, suggesting it could be a potential target for HCC treatment.
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Background: Hepatitis B virus (HBV) is one of the major pathogens of human liver disease. Studies have shown that HBV X protein (HBx) plays an important role in promoting viral gene expression and replication. In this study we performed a global proteomic profiling to identify the downstream functional proteins of HBx, thereby detecting the mechanisms of action of HBx on virion replication.

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