ArticlePloS one2016
Elevated Cellular PD1/PD-L1 Expression Confers Acquired Resistance to Cisplatin in Small Cell Lung Cancer Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 72 citations in OpenAlex.
- The immune signatures predict gastric/gastroesophageal junction cancer response to first-line anti-PD-1 blockade or chemotherapy.BMC cancer · 2025Trial
- Article
- NAT10 promotes cisplatin resistance and immune escape by increasing the expression of DUSP1 and PD-L1 in gastric cancer.Cell death discovery · 2026Article
- Senescence‑associated IL‑33 secretion undermines sorafenib efficacy in hepatocellular carcinoma via immune evasion.Oncology reports · 2025Article
- Molecular Features and Actionable Gene Targets of Testicular Germ Cell Tumors in a Real-World Setting.International journal of molecular sciences · 2025Article
- Predicting Treatment Outcomes in Glioblastoma: A Risk Score Model for TMZ Resistance and Immune Checkpoint Inhibition.Biology · 2025Article
- A novel therapeutic approach targeting PD-L1 in HNSCC and bone marrow-derived mesenchymal stem cells hampers pro-metastatic features in vitro: perspectives for blocking tumor-stroma communication and signaling.Cell communication and signaling : CCS · 2025Article
- Development of selective ssDNA micro-probe for PD1 detection as a novel strategy for cancer imaging.Scientific reports · 2024Article
- Small cells - big issues: biological implications and preclinical advancements in small cell lung cancer.Molecular cancer · 2024Review
- Article
- Impact of glucose metabolism on PD-L1 expression in sorafenib-resistant hepatocellular carcinoma cells.Scientific reports · 2024Article
- Exploring the Impact of Exosomal Cargos on Osteosarcoma Progression: Insights into Therapeutic Potential.International journal of molecular sciences · 2024Review
- Novel Therapeutic Options for Small Cell Lung Cancer.Current oncology reports · 2023Review
- Dual inhibition of IDO1/TDO2 enhances anti-tumor immunity in platinum-resistant non-small cell lung cancer.Cancer & metabolism · 2023Article
- PD-L1 expression and smoke exposure as biomarkers for optimizing adjuvant therapy for patients with resected limited-stage small-cell lung carcinoma.Genes & diseases · 2023Article
- DNA methyltransferase-1 in acute myeloid leukaemia: beyond the maintenance of DNA methylation.Annals of medicine · 2022Review
- Cooperation between chemotherapy and immune checkpoint blockade to enhance anti-tumour T cell immunity in oesophageal adenocarcinoma.Translational oncology · 2022Article
- PD-1 blockade enhances chemotherapy toxicity in oesophageal adenocarcinoma.Scientific reports · 2022Article
- An acetonic extract and secondary metabolites from the endolichenic fungusFrontiers in pharmacology · 2022Article
- The ubiquitin E3 ligase FBXO22 degrades PD-L1 and sensitizes cancer cells to DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Although small cell lung cancer (SCLC) is highly responsive to chemotherapies (e.g., cisplatin-etoposide doublet), virtually almost all responsive SCLC patients experience disease recurrence characterized by drug resistance. The mechanisms underlying cisplatin resistance remain elusive. Here we report that cell-intrinsic expression of PD1 and PD-L1, two immune checkpoints, is required for sustained expansion of SCLC cells under cisplatin selection. Indeed, PD1 and PD-L1 were expressed at a higher level in lung cancer cell lines, tumor tissues, and importantly, in SCLC cells resistant to cisplatin (H69R, H82R), when compared to respective controls. Genetic abrogation of PD1 and PD-L1 in H69R and H82R cells decreased their proliferation rate, and restored their sensitivity to cisplatin. Mechanistically, PD-L1 upregulation in H69R and H82R cells was attributed to the overexpression of DNA methyltransferase 1 (DNMT1) or receptor tyrosine kinase KIT, as knockdown of DNMT1 or KIT in H69R and H82R cells led to PD-L1 downregulation. Consequently, combined knockdown of PD-L1 with KIT or DNMT1 resulted in more pronounced inhibition of H69R and H82R cell growth. Thus, cell intrinsic PD1/PD-L1 signaling may be a predictor for poor efficacy of cisplatin treatment, and targeting the cellular PD1/PD-L1 axis may improve chemosensitization of aggressive SCLC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.