Background: Hepatitis B virus X protein (HBx) is an indispensable progression factor in Hepatocellular Carcinoma (HCC). CCL15 could be a peculiar proteomic biomarker of HCC with tumorigenesis and tumor invasion.
Objective: The aim of the study was to explore the relationship between HBx and CCL15 expression in HCC.
Methods: HBV-positive HCC pathological tissue samples and corresponding adjacent non-tumor liver tissues were collected. The expression of HBx and CCL15 was analyzed by immunohistochemistry, real-time Polymerase Chain Reaction (PCR), and western blot analysis in tissues or in vitro.
Results: The levels of CCL15 mRNA and protein expression in HCC samples were observably higher than those of adjacent non-tumor liver tissues. The CCL15 was significantly associated with the expression of HBx in HBV-positive HCC samples. The up-regulation of HBx induced CCL15 expression in vitro. The high expression score of CCL15 was significant associated with the poor prognosis of HCC patients.
Conclusion: The CCL15 expression was observably associated with HBx in HCC patients. The CCL15 may be considered as an indicator in the clinical management of HBV-associated HCC.
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http://dx.doi.org/10.2174/1871520621666210302083407 | DOI Listing |
Cancer Lett
December 2024
Department of Laboratory, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, PR China. Electronic address:
Hepatocellular carcinoma (HCC) is a lethal malignancy characterized by rapid growth. The interaction between tumor cells and cancer-associated fibroblasts (CAFs) significantly influences HCC progression. CCL15, a CC chemokine family member, is predominantly expressed in HCC and strongly correlates with tumor size, indicating its critical role in HCC growth.
View Article and Find Full Text PDFComput Biol Chem
December 2024
Hefei Cancer Hospital of CAS; Institute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences (CAS), Hefei 230031, China; School of Mathematics and Computer Science, Tongling University, Tongling 244061, China. Electronic address:
Tumor microenvironent contains prognostic molecular markers and therapeutic targets from different cellular sources, which are still not fully revealed in the resistance and recurrence after radiotherapy for rectal cancer. By integrating the scRNA-seq data, we deconvoluted the bulk transcriptomics of rectal cancer collected before preoperative neoadjuvant radiotherapy (nRT) into fractions and gene expression of the six cell types. The inferred cell-type-associated DEGs, abbreviated as caDEGs, of myeloid and stromal cells were enriched for overlapping yet unique biological processes including immunity, angiogenesis, and metabolism, respectively.
View Article and Find Full Text PDFJ Cell Mol Med
October 2024
Department of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Front Immunol
September 2024
Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD, United States.
Background: Limited data are available describing the effects of SARS-CoV-2 breakthrough infections on the plasma proteome.
Methods: PCR-positive SARS-CoV-2 patients, enrolled in a natural history study, underwent analysis of the plasma proteome. A prospective cohort of 66 unvaccinated and 24 vaccinated persons with different degrees of infection severity were evaluated acutely (within 40 days of symptom onset), and at three and ten months.
Acta Pharm Sin B
August 2024
Tongji School of Pharmacy, Huazhong University of Science and Technology, Wuhan 430030, China.
SMAD4 deficiency in colorectal cancer (CRC) is highly correlated with liver metastasis and high mortality, yet there are few effective precision therapies available. Here, we show that CCR1-granulocytic myeloid-derived suppressor cells (G-MDSCs) are highly infiltrated in SMAD4-deficient CRC CCL15/CCR1 and CCL9/CCR1 axis in clinical specimens and mouse models, respectively. The excessive TGF-, secreted by tumor-infiltrated CCR1-G-MDSCs, suppresses the immune response of cytotoxic T lymphocytes (CTLs), thus facilitating metastasis.
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