B7‐1 and programmed cell death‐ligand 1 in primary and lymph node metastasis lesions of non‐small cell lung carcinoma

Yamada, Takehiro; Miki, Yasuhiro; Suzuki, Miho; Kondoh, Osamu; Saito, Ryoko; Ono, Koji; Okada, Yoshinori; Sasano, Hironobu

doi:10.1002/cam4.4444

Cited by 5 publications

(2 citation statements)

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“…PD-1, as an inhibitory co-receptor, can inhibit the activity of T cells after interacting with PD-L1, making the cells arrest in the G0/G1 phase, thus inhibiting the proliferation and inducing the apoptosis of T cells. In tumor patients, high expression of PD-L1 can enhance the ability of tumor metastasis, leading to increased mortality of patients [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Analysis of the Role and Mechanism of ZEB1 in Regulating Cervical Carcinoma Progression via Modulating PD-1/PD-L1 Checkpoint

Lin

Wang

2022

Computational and Mathematical Methods in Medicine

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Background. Cervical carcinoma (CC) is a common and highly malignant tumor in women. The involvement of zinc finger E-box binding homeobox 1 (ZEB1) in many kinds of tumors has been well-documented; however, its role and mechanism in CC remain to be clarified. Objective. This study investigated the mechanism of ZEB1 in modulating the growth and metastasis of CC cells. Methods. The expression of ZEB1 in CC tissues and adjacent normal counterparts was determined by reverse transcription-polymerase chain reaction (RT-PCR). The correlation between ZEB1 and patient clinicopathological indexes was analyzed. In vitro, gain and loss functions of ZEB1 were performed in C-33A and HeLa cell lines. The proliferation, migration, and invasion of CC cells were detected by Cell Counting Kit-8 (CCK-8) assay and transwell assay, respectively. The expression levels of apoptosis-related proteins such as BCL2-associated X (Bax), B-cell lymphoma-2 (Bcl2), and Caspase-3, as well as epithelial-mesenchymal transition (EMT)-associated proteins including E-cadherin, Vimentin, and Snail, were measured by Western blotting. In addition, the targeting relationship between ZEB1 and programmed death 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) was predicted by bioinformatics and further verified by dual-luciferase reporter assay. Results. ZEB1 was significantly up-regulated in CC tissues compared with normal counterparts. ZEB1 overexpression promoted the migration, proliferation, and invasion of CC cells and inhibited apoptosis, while knocking down ZEB1 contributed to the opposite effects. In addition, experiments on related mechanisms confirmed that ZEB1 targeted the 3’EUTR terminal of PD-1/PD-L1 and negatively regulated its expression. And an interaction between ZEB1 and PD-1/PD-L1 was identified. Conclusion. ZEB1 can promote the proliferation and metastasis of CC cells via modulating the PD-1/PD-L1 checkpoint.

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Section: Introductionmentioning

confidence: 99%

Analysis of the Role and Mechanism of ZEB1 in Regulating Cervical Carcinoma Progression via Modulating PD-1/PD-L1 Checkpoint

Lin

Wang

2022

Computational and Mathematical Methods in Medicine

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“…Some authors suggest that microenvironment characteristics may contribute to the differences in expression between PT and LNM, such as infiltration of cytotoxic T lymphocytes were considered to play a pivotal role in higher PD-L1 positivity by tumor positive score status found in metastatic sites[ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Assessment of programmed death-ligand 1 expression in primary tumors and paired lymph node metastases of gastric adenocarcinoma

Coimbra,

Pereira,

Cardili

et al. 2024

World J Gastrointest Oncol

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BACKGROUND Anti-programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) immunotherapy has demonstrated promising results on gastric cancer (GC). However, PD-L1 can express differently between metastatic sites and primary tumors (PT). AIM To compare PD-L1 status in PT and matched lymph node metastases (LNM) of GC patients and to determine the correlation between the PD-L1 status and clinicopathological characteristics. METHODS We retrospectively reviewed 284 GC patients who underwent D2-gastrectomy. PD-L1 was evaluated by immunohistochemistry (clone SP142) using the combined positive score. All PD-L1+ PT staged as pN+ were also tested for PD-L1 expression in their LNM. PD-L1(-) GC with pN+ served as the comparison group. RESULTS Among 284 GC patients included, 45 had PD-L1+ PT and 24 of them had pN+. For comparison, 44 PD-L1(-) cases with pN+ were included (sample loss of 4 cases). Of the PD-L1+ PT, 54.2% (13/24 cases) were also PD-L1+ in the LNM. Regarding PD-L1(-) PT, 9.1% (4/44) had PD-L1+ in the LNM. The agreement between PT and LNM had a kappa value of 0.483. Larger tumor size and moderate/severe peritumoral inflammatory response were associated with PD-L1 positivity in both sites. There was no statistical difference in overall survival for PT and LNM according to the PD-L1 status (P = 0.166 and P = 0.837, respectively). CONCLUSION Intra-patient heterogeneity in PD-L1 expression was observed between the PT and matched LNM. This disagreement in PD-L1 status may emphasize the importance of considering different tumor sites for analyses to select patients for immunotherapy.

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