Publications by authors named "Jin-Pei Liu"
Background: The activation of hepatic stellate cells (HSCs) has been emphasized as a leading event of the pathogenesis of liver cirrhosis, while the exact mechanism of its activation is largely unknown. Furthermore, the novel non-invasive predictors of prognosis in cirrhotic patients warrant more exploration. miR-541 has been identified as a tumor suppressor in hepatocellular carcinoma and a regulator of fibrotic disease, such as lung fibrosis and renal fibrosis.
View Article and Find Full Text PDFColorectal cancer (CRC) is the second leading cause of cancer-related deaths worldwide, and its incidence continues to rise, particularly in developing countries. The advent of immune checkpoint inhibitors (ICIs) has represented a significant advancement in CRC treatment. Deficient mismatch repair (dMMR) or high microsatellite instability (MSI-H) serves as a biomarker for immunotherapy, with dMMR/MSI-H CRC exhibiting significantly better response rates to immunotherapy compared to proficient mismatch repair (pMMR)or microsatellite stable (MSS) CRC.
View Article and Find Full Text PDFArticle Synopsis
- This study explores how autophagy influences the growth and resistance of hepatocellular carcinoma (HCC) cells to sorafenib, focusing on the role of miR-541 in this process.
- Researchers used various techniques to show that lower levels of miR-541 in HCC tissues are linked to aggressive cancer traits and poorer patient outcomes, while increasing miR-541 can inhibit HCC cell growth and autophagy.
- The findings suggest that targeting the miR-541-ATG2A/RAB1B pathway could enhance the effectiveness of sorafenib for HCC treatment and potentially improve patient survival.
Src homology region 2 (SH2) domain-containing phosphatase 1 (SHP-1, also known as PTPN6) is a nonreceptor protein tyrosine phosphatase that acts as a negative regulator of inflammation. Emerging evidence indicates that SHP-1 plays a role in inhibiting the progression of hepatocellular carcinoma (HCC). However, the role of SHP-1 in hepatocarcinogenesis remains unknown.
View Article and Find Full Text PDFBackground: Our previous study has demonstrated that hepatocyte nuclear factor 1α (HNF1α) exerts potent therapeutic effects on hepatocellular carcinoma (HCC). However, the molecular mechanisms by which HNF1α reverses HCC malignancy need to be further elucidated.
Methods: lncRNA microarray was performed to identify the long noncoding RNAs (lncRNAs) regulated by HNF1α.