Ask about this productRelated genes to: PDCD2L antibody
- Gene:
- PDCD2L NIH gene
- Name:
- programmed cell death 2 like
- Previous symbol:
- -
- Synonyms:
- MGC13096
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-31
- Date modifiied:
- 2016-06-22
Related products to: PDCD2L antibody
Related articles to: PDCD2L antibody
- BackgroundGastric cancer is the 4th most common and 3rd deadliest cancer worldwide. Research has shown that PDCD2-like (PDCD2L) is elevated in several tumors.ObjectiveTo explore the relationship between PDCD2L expression and gastric cancer prognosis and its function in gastric cancer.MethodsImmunohistochemical staining and immunoblotting were performed to examine the expression of PDCD2L. The effect of PDCD2L on gastric cancer cells were evaluated by a series of in vitro cellular function experiments and in vivo proliferation experiments.ResultsPDCD2L was found to be overexpressed in gastric cancer tissues compared to non-tumor tissues, and its higher levels were associated with worse prognosis. In vitro experiments showed that reducing PDCD2L expression in gastric cancer cells led to decreased proliferation, migration, and invasion, with a similar effect observed in animal models. Knockdown of PDCD2L also resulted in lower expression of cell cycle- and motility-related proteins, while upregulation of PDCD2L had the opposite effect. Additionally, NGS analysis revealed that PDCD2L knockdown reduced the expression of RFX1, a gene linked to cell proliferation and migration, suggesting that PDCD2L and RFX1 together promote cancer progression.ConclusionPDCD2L could serve as a biomarker for gastric cancer prognosis and a potential therapeutic target. - Source: PubMed
Publication date: 2025/09/02
Sun Ding-PingChang Chun-ChaoHuang Hsuan-YiKang Nai-WengHseu You-ChengTian Yu-FengFang Chia-LangLin Kai-Yuan - Toys are us (Trus) is the Drosophila melanogaster ortholog of mammalian Programmed Cell Death 2-Like (PDCD2L), a protein that has been implicated in ribosome biogenesis, cell cycle regulation, and oncogenesis. In this study, we examined the function of Trus during Drosophila development. CRISPR/Cas9 generated null mutations in trus lead to partial embryonic lethality, significant larval developmental delay, and complete pre-pupal lethality. In mutant larvae, we found decreased cell proliferation and growth defects in the brain and imaginal discs. Mapping relevant tissues for Trus function using trus RNAi and trus mutant rescue experiments revealed that imaginal disc defects are primarily responsible for the developmental delay, while the pre-pupal lethality is likely associated with faulty central nervous system (CNS) development. Examination of the molecular mechanism behind the developmental delay phenotype revealed that trus mutations induce the Xrp1-Dilp8 ribosomal stress-response in growth-impaired imaginal discs, and this signaling pathway attenuates production of the hormone ecdysone in the prothoracic gland. Additional Tap-tagging and mass spectrometry of components in Trus complexes isolated from Drosophila Kc cells identified Ribosomal protein subunit 2 (RpS2), which is coded by string of pearls (sop) in Drosophila, and Eukaryotic translation elongation factor 1 alpha 1 (eEF1α1) as interacting factors. We discuss the implication of these findings with respect to the similarity and differences in trus genetic null mutant phenotypes compared to the haplo-insufficiency phenotypes produced by heterozygosity for mutants in Minute genes and other genes involved in ribosome biogenesis. - Source: PubMed
Publication date: 2025/06/27
Takada SaekoBolkan Bonnie JO'Connor MaryJaneGoldberg MichaelO'Connor Michael B - Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, with the characteristics of high mortality and low 5-year survival rate. The potential role of BTF3 and PDCD2L in HCC remains unclear. Our study found that BTF3 expression was upregulated in hepatocellular carcinoma tissues, and its high expression was associated with poor prognosis. Knockdown of BTF3 significantly inhibited proliferation and promoted apoptosis of hepatocellular carcinoma cells by cell function assay. Mechanistically, BTF3 plays an oncogenic role by regulating the transcriptional expression of PDCD2L, which promotes proliferation and inhibits apoptosis of HCC cells by restraining the p53 pathway. In conclusion, our results suggest that BTF3 induces malignant progression of HCC by acting as a transcription factor that promotes the transcription of PDCD2L and influences the p53 pathway and that the BTF3/PDCD2L/P53 axis may be a future therapeutic strategy for HCC patients. - Source: PubMed
Publication date: 2024/12/20
Kong MinyuShi XiaoyiGao JieGuo Wenzhi - Nanoplastics (NPs) can penetrate the intestinal barrier of organisms and accumulate in the liver, thereby inducing hepatocyte apoptosis. However, the underlying mechanisms remain incompletely elucidated. This study examined the effects of PS-NPs exposure on hepatocyte apoptosis and revealed the role of cell cycle arrest and mitophagy. The C57BL/6 mice were administered a diet containing 100 nm and 500 nm PS-NPs at a concentration of 0.1 g/kg for 180 days, respectively. TUNEL staining confirmed that 100 nm PS-NPs induced more pronounced apoptosis compared to 500 nm PS-NPs in mouse liver. Mechanistically, proteomic analysis revealed that Pdcd2l, associated with the S phase of cell cycle and apoptosis, exhibited the highest fold changes among all detected proteins in 100 nm and 500 nm PS-NPs exposure groups. Notably, the expression of Tbc1d17, Bcl2l13, and Pgam5 involved in mitophagosome formation in mouse liver was upregulated by 100 nm PS-NPs but not by 500 nm PS-NPs; moreover, mitophagosomes were observed in HepG2 cells exposed to 100 nm PS-NPs. Additionally, 100 nm PS-NPs internalized by HepG2 cells could penetrate lysosomes. The protein levels of Igf2r and Rab7a were altered, and mRNA expression was increased in mouse liver, suggesting 100 nm PS-NPs, but not 500 nm PS-NPs, impaired lysosomal function and subsequently inhibited mitophagy degradation. Collectively, 500 nm PS-NPs induced Pdcd2l-mediated cell cycle arrest, thereby exacerbating hepatocyte apoptosis; while 100 nm PS-NPs not only triggered similar levels of cell cycle arrest as 500 nm PS-NPs, but also disrupted mitophagy, which was also associated with hepatocyte apoptosis. - Source: PubMed
Publication date: 2024/11/12
Lu Yan-YangHua WeizhenSun YiqiongLu LuRen HongyunHuang Qingyu - Toys are us (Trus) is the ortholog of mammalian Programmed Cell Death 2-Like (PDCD2L), a protein that has been implicated in ribosome biogenesis, cell cycle regulation, and oncogenesis. In this study, we examined the function of Trus during development. CRISPR/Cas9 generated null mutations in lead to partial embryonic lethality, significant larval developmental delay, and complete pre-pupal lethality. In mutant larvae, we found decreased cell proliferation and growth defects in the brain and imaginal discs. Mapping relevant tissues for Trus function using and mutant rescue experiments revealed that imaginal disc defects are primarily responsible for the developmental delay, while the pre-pupal lethality is likely associated with faulty central nervous system (CNS) development. Examination of the molecular mechanism behind the developmental delay phenotype revealed that mutations induce the Xrp1-Dilp8 ribosomal stress-response in growth-impaired imaginal discs, and this signaling pathway attenuates production of the hormone ecdysone in the prothoracic gland. Additional Tap-tagging and mass spectrometry of components in Trus complexes isolated from Kc cells identified Ribosomal protein subunit 2 (RpS2), which is coded by in , and Eukaryotic translation elongation factor 1 alpha 1 (eEF1α1) as interacting factors. We discuss the implication of these findings with respect to the similarity and differences in genetic null mutant phenotypes compared to the haplo-insufficiency phenotypes produced by heterozygosity for mutants in Minute genes and other genes involved in ribosome biogenesis. - Source: PubMed
Publication date: 2024/10/26
Takada SaekoBolkan Bonnie JO'Connor MaryJaneGoldberg MichaelO'Connor Michael B