Overexpression of Phosphoserine Aminotransferase 1 (PSAT1) Predicts Poor Prognosis and Associates with Tumor Progression in Human Esophageal Squamous Cell Carcinoma

Liu, Bingyan; Jia, Yiping; Chen, Yan; Wu, Shaoqiu; Jiang, Haixiang; Sun, Xianjun; Ma, Jun; Yin, Xiaoxing; Mao, Aiwu; Shang, Ming

doi:10.1159/000445633

Cited by 53 publications

(51 citation statements)

References 28 publications

(26 reference statements)

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“…During the physio-pathological process of EMT, epithelial cells interact with surrounding mesenchymal cells, and obtain certain mesenchymal phenotypes, including changes in morphology, polarity, surface markers, and related transcription factors [36][37][38][39][40][41]. Once the cancer cells obtain mesenchymal phenotypes, they gain the ability to migrate into the stroma or migrate to distant sites and organs, and finally contribute to tumor metastasis and recurrence [42,43].…”

Section: Discussionmentioning

confidence: 99%

PD-L1 Expression Promotes Epithelial to Mesenchymal Transition in Human Esophageal Cancer

Chen

Xiong

et al. 2017

Cell Physiol Biochem

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Background/Aims: PD-L1 (Programmed cell death 1 ligand 1, PD-L1), an essential immune checkpoint molecule in the tumor microenvironment, is an important target for cancer immunotherapy. We have previously reported that its expression in human gastric and esophageal cancer tissues is significantly associated with cancer progression and patients' postoperative prognoses. Its expression in cancer cells is well known to inhibit the T cellmediated anti-tumor response, and this mechanism of action has been targeted for cancer immunotherapy. As of now, the autonomous effect of PD-L1 on cancer cells is not well understood, thus our present study aimed to examine the role of PD-L1 intervention in cellular biological functions, especially epithelial to mesenchymal transition (EMT), of the human esophageal cancer cell line, Eca-109 cells. Methods: Immunohistochemistry assay was used to investigate the correlation between expression of PD-L1 and EMT markers in human esophageal cancer tissues. Intervention of PD-L1 by using RNAi and over-expression methods were used to study the role of PD-L1 in regulation of biological behaviors and EMT in Eca-109 cells. Results: Our clinical and pathological data demonstrated that tumor samples in the EMT positive subgroup had higher PD-L1 expression than those in the EMT negative subgroup. By manipulating PD-L1 expression in Eca-109 cells either through ablation or overexpression of wild type and the cytoplasmic domain-truncated mutant, we demonstrated that PD-L1 expression significantly promoted the cell viability, migration and EMT phenotype. Furthermore, our study also indicated that PD-1 fusion protein mediated stimulation of PD-L1 and the cytoplasmic domain of PD-L1 played a critical role in promoting EMT phenotype of Eca-109 cells, thereby suggesting that PD-1 receptor usually by triggering the reverse signaling can effect PD-L1 mediated regulation of esophageal cancer cell response. Conclusion: Our present study reveals a tumor cell-autonomous role of PD-L1 signaling in promoting EMT in human esophageal cancer.L. Chen and Y. Xiong contributed equally to this work.

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Section: Discussionmentioning

confidence: 99%

PD-L1 Expression Promotes Epithelial to Mesenchymal Transition in Human Esophageal Cancer

Chen

Xiong

et al. 2017

Cell Physiol Biochem

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“…IHC staining was performed using a standard streptavidin-biotin-peroxidase complex method as previously described [16]. In brief, paraffin sections were deparaffinized and hydrated.…”

Section: Methodsmentioning

confidence: 99%

Elevated FOXC2 Expression Promotes Invasion of HCC Cell Lines and is Associated with Poor Prognosis in Hepatocellular Carcinoma

Yang

Liu

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Increasing evidence has indicated that Forkhead box protein C2 (FOXC2) plays an important role in carcinogenesis. However, the expression and the role of FOXC2 in hepatocellular carcinoma (HCC) have not been extensively studied. Methods: FOXC2 expression was analyzed by quantitative real-time polymerase chain reaction, Western blot analysis and immunohistochemistry in HCC tissue and cells. The relationship between FOXC2 expression and patient clinical significance and survival were assessed by Pearson’s correlation and Kaplan-Meier analysis, respectively. Cell proliferation assays, colony formation assays, flow cytometric analysis and Transwell assays were employed to measure the effects of FOXC2 on HCC cells in vitro. Results: The expression of FOXC2 was increased in HCC tissue, and high FOXC2 expression was associated with worse patient survival. Knockdown of FOXC2 inhibited HCC cell growth, migration, and invasion in vitro, as well as tumor growth. Furthermore, we found that activation of AKT-mediated MMP-2 and MMP-9 was involved in FOXC2 promoting an aggressive phenotype. Conclusions: Taken together, these findings demonstrate that FOXC2 is upregulated in HCC tissue and is associated with tumor size, vascular invasion and advanced TNM stage. Further investigation suggested that FOXC2 may play a vital role in promoting proliferation and invasion in HCC and serves as a novel therapeutic target in HCC.

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“…Actually, similar with GLDC, some other glycine/serine metabolism enzymes such as SHMT1/2, PSPH, and PSAT1, are involved in both tumorigenesis [9] and metastasis [14,37,38]. And increased expression of these enzymes in tumors predict poor prognosis [38,39]. These observations provide evidences for the notion that metabolic reprogramming, especially glycine/serine metabolic reprogramming in cancer cells might be crucial for metastasis [40].…”

Section: Discussionmentioning

confidence: 79%

“…In another hand, increased proportion of CSCs in primary tumor tissues mediated by increased GLDC would also promote metastasis. Actually, similar with GLDC, some other glycine/serine metabolism enzymes such as SHMT1/2, PSPH, and PSAT1, are involved in both tumorigenesis [9] and metastasis [14,37,38]. And increased expression of these enzymes in tumors predict poor prognosis [38,39].…”

Section: Discussionmentioning

confidence: 99%

OGT-mediated O-GlcNAcylation on GLDC promotes metastasis in cervical cancer

Cai¹,

Jin²,

Zhu³

et al. 2018

Oncotarget

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Glycine decarboxylase (GLDC) is one of the glycine metabolic enzymes and was reported as a oncogene involved in tumorigenesis of non-small cell lung cancer. However, the function of GLDC in cervical cancer remains unclear. In this study, we determined the increased expression of GLDC in cervical cancer tissues and cell lines. The clinical pathological characters of GLDC revealed that increased GLDC expression was involved in cervical cancer metastasis. Further in vitro experiments confi rmed the promotion of GLDC on cervical cancer metastasis. Furthermore, we found that OGT interacted with GLDC and modifi ed GLDC with O-GlcNAcylation in cervical cancer cell lines. In addition, the O-GlcNAcylation of GLDC greatly enhanced its promotion on migration and invasion in vitro and in vivo. The clinical data further demonstrated the promotion of GLDC and OGT on cervical cancer metastasis, and showed that OGT worsened the prognosis of GLDC High patients. Collectively, this study identifi ed OGT-mediated O-GlcNAcylation on GLDC as an essential regulatory mechanism for promoting cervical cancer metastasis, and provided a therapeutic target for metastatic cervical cancer. www.impactjournals.com/oncotarget/

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Overexpression of Phosphoserine Aminotransferase 1 (PSAT1) Predicts Poor Prognosis and Associates with Tumor Progression in Human Esophageal Squamous Cell Carcinoma

Cited by 53 publications

References 28 publications

PD-L1 Expression Promotes Epithelial to Mesenchymal Transition in Human Esophageal Cancer

PD-L1 Expression Promotes Epithelial to Mesenchymal Transition in Human Esophageal Cancer

Elevated FOXC2 Expression Promotes Invasion of HCC Cell Lines and is Associated with Poor Prognosis in Hepatocellular Carcinoma

OGT-mediated O-GlcNAcylation on GLDC promotes metastasis in cervical cancer

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