TY  - JOUR
AB  - Checkpoint immunotherapy is capable of unleashing T cells for controlling tumor, whereas it is destroyed by immunosuppressive myeloid cell. Apoprotein E (APOE) refers to a ligand in terms of the members of low-density lipoprotein (LDL) receptor family for mediating Apoprotein B-involving atherogenic lipoprotein clearance. Besides, tumor-infiltration macrophage can express APOE. The present study reported Apoe-/- mice to exhibit higher resistance toward the development of three types of carcinomas as compared with mice with wild type and to have greater responses to αPD-1 (anti-PD-1) immunotherapy. Moreover, treatment by exploiting APOE inhibitor (COG 133TFA, αAPOE) was capable of curbing tumor development and fostering regression if in combination of αPD-1. According to single-cell RNA sequencing (scRNA-seq), Apoe deletion was correlated with the decline of C1QC+ and CCR2+ macrophage within tumor infiltration, and mass spectrometry results noticeably showed down-regulated the number of M2 macrophages as well. Furthermore, APOE expression in cancer patients resistant to αPD-1 treatment significantly exceeded that in the sensitive group. For this reason, APOE is likely to be targeted for modifying tumor macrophage infiltrate and augmenting checkpoint immunotherapy.
AU  - Hui, B.*
AU  - Lu, C.*
AU  - Li, H.*
AU  - Hao, X.*
AU  - Liu, H.*
AU  - Zhuo, D.*
AU  - Wang, Q.
AU  - Li, Z.*
AU  - Liu, L.*
AU  - Wang, X.*
AU  - Gu, Y.*
AU  - Tang, W.*
C1  - 66187
C2  - 52623
SP  - 5230-5240
TI  - Inhibition of APOE potentiates immune checkpoint therapy for cancer.
JO  - Int. J. Biol. Sci.
VL  - 18
IS  - 14
PY  - 2022
SN  - 1449-2288
ER  - 

TY  - JOUR
AB  - Circular RNAs (circRNAs) is a novel class of non-coding RNAs resulting from the non-canonical splicing of linear pre-mRNAs. However, the role of circRNAs in gastric cancer (GC) remains indistinct. This study aims to explore their potential modulation in GC and its prognostic value. We first screen for circRNA expression patterns in GC through GC and adjacent noncancerous tissues by microarray. Based on the bioinformatics analysis of the microarray data, we screened out a novel circRNA, circ-PTPDC1. Then we demonstrated that circ-PTPDC1 was up-regulated in GC cells, tissues, and serum. Its overexpression was positively correlated with age, invasion depth, advanced clinical stages, and worse survival in patients with GC. We further revealed that circ-PTPDC1 promotes the proliferation, migration, and invasion of GC cell lines via sponging miR-139-3p by regulating ELK1. Importantly, we identified that circ-PTPDC1 promotes tumor upgrowth and metabasis in vivo. Additionally, we established its prognostic prediction model based on the follow-up data of the patients. Our study revealed a novel regulatory mechanism and a comprehensive landscape of circ-PTPDC1 in GC, suggesting that circ-PTPDC1 has the potential to be a biomarker for early detection and prognostic prediction of GC.
AU  - Li, Z.*
AU  - Cheng, Y.*
AU  - Fu, K.*
AU  - Lin, Q.*
AU  - Zhao, T.
AU  - Tang, W.*
AU  - Xi, L.*
AU  - Sheng, L.*
AU  - Zhang, H.*
AU  - Sun, Y.*
C1  - 63656
C2  - 51571
SP  - 4285-4304
TI  - Circ-PTPDC1 promotes the progression of gastric cancer through sponging Mir-139-3p by regulating ELK1 and functions as a prognostic biomarker.
JO  - Int. J. Biol. Sci.
VL  - 17
IS  - 15
PY  - 2021
SN  - 1449-2288
ER  -