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Molecular profiling analysis for colorectal cancer patients with Pi-Xu or Shi-Re syndrome
Xinbing Sui,Yong Guo,Wei Ni,Haiyan Jin,Haoming Lin,Tian Xie 한국한의학연구원 2019 Integrative Medicine Research Vol.8 No.1
Background: Traditional Chinese medicine (TCM) syndromes (ZHENG in Chinese) constitute the basis of understanding the disorders of patients and guiding the use of the Chinese herbs. Colorectal cancer is divided into various subtypes mainly according to the ZHENG identification. Objective: We aimed to determine the molecular basis underlying Pi-Xu (spleen deficiency) and Shi-Re (dampness-heat) ZHENG that are commonly found in colorectal cancer patients. Methods: About 80 colorectal cancer patients, including 47 Pi-Xu ZHENG and 33 Shi-Re ZHENG were enrolled. Blood and tissue samples of these patients were available for protein and mRNA expression. The protein expression was determined by Immunohistochemistry (IHC) staining and mRNA profiling was detected by expression microarray. Furthermore, mRNA fold change was evaluated by qRT-PCR. Results: The colorectal cancer patients with Shi-Re ZHENG had a poor prognosis, compared with Pi-Xu ZHENG (95% CI: 0.05–0.33; p < 0.0001). Moreover, there was a significant difference in protein expression levels (especially for mutant TP53, PCNA, PD-L1 and Ki-67) among Pi-Xu and Shi-Re ZHENG (p < 0.01). Meanwhile, mRNA expression (especially for wild type TP53, KDM6A, PCNA, PD-L1, Ki-67, CCL-2, IL-1a and COX-2) was also remarkably different between Pi-Xu and Shi-Re groups (p < 0.01). Conclusion: Our results suggest that Shi-Re ZHENG conditions may contribute to poor overall survival in patients with colorectal cancer. Compared with Pi-Xu ZHENG, high expression of mutant TP53, PCNA, PD-L1, Ki-67, CCL-2, IL-1a and COX-2 may serve as potential biomarkers for diagnosis and prognosis of colorectal cancer patients displayed Shi-Re ZHENG.
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Wenbin Li,Yue Zhu,Kelin Zhang,Xianhuan Yu,Haoming Lin,Wenrui Wu,Yaorong Peng,Jian Sun 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-
In recent years, the deoxycytidine analogue gemcitabine (2′,2′,-difluorodeoxycytidine) has become the first-line chemotherapeutic agent for patients with pancreatic cancer. However, due to the intrinsic resistance of pancreatic cancer cells, gemcitabine-based chemotherapy yields limited disease control, with >85% disease progression at 6 months from diagnosis. Therefore, elucidating the mechanisms of chemoresistance is a critical step in improving cancer therapy, especially for the treatment of pancreatic cancer. We show PROM2, a transmembrane glycoprotein, is ubiquitously upregulated in pancreatic cancer cell. We also found higher PROM2 expression is associated with shortened overall and disease-free survival times in patients diagnosed with pancreatic cancer. We provide evidence that PROM2 promotes chemoresistance to gemcitabine both in vivo and in vitro. Mechanistically, we demonstrate that PROM2 could directly interacted with Akt and activates the Akt signaling pathway, which thus inhibiting gemcitabineinduced apoptosis. As further evidence, we show PROM2 expression and Akt phosphorylation both promote gemcitabine chemoresistance, and cause poorer survival in clinical samples with pancreatic cancer. Combining gemcitabine with the Akt inhibitor MK-2206 facilitated significant tumor shrinkage and dramatically elevated the survival status in mice xenografted with pancreatic cancer cells. Our findings not only establish PROM2 as a novel positive regulator of the Akt signaling pathway and a candidate prognostic indicator of gemcitabine response, but also provide a neo-therapeutic approach for patients resistant to gemcitabine treatment.
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