ArticleAmerican journal of cancer research2019
KLK11 suppresses cellular proliferation via inhibition of Wnt/β-catenin signaling pathway in esophageal squamous cell carcinoma.
Article in American journal of cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 10 citations in OpenAlex.
- PRSS23 functions downstream of ZEB1 to promote esophageal squamous cell carcinoma progression by driving M2 polarization of tumor associated macrophages.Molecular and cellular biochemistry · 2026Article
- CD8 + T-Cell-Related Genes: Deciphering Their Role in the Pancreatic Adenocarcinoma TME and Their Effect on Prognosis.Digestive diseases and sciences · 2025Article
- Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway.Thoracic cancer · 2023Article
- A Pair of Prognostic Biomarkers in Triple-Negative Breast Cancer: KLK10 and KLK11 mRNA Expression.Life (Basel, Switzerland) · 2022Article
- PNMA5 accelerated cellular proliferation, invasion and migration in colorectal cancer.American journal of translational research · 2022Article
- A computational method for large-scale identification of esophageal cancer-related genes.Frontiers in oncology · 2022Article
- KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy.BMC cardiovascular disorders · 2021Article
- TGIF1 plays a carcinogenic role in esophageal squamous cell carcinoma through the Wnt/β‑catenin and Akt/mTOR signaling pathways.International journal of molecular medicine · 2021Article
- KLK11 acts as a tumor-inhibitor in laryngeal squamous cell carcinoma through the inactivation of Akt/Wnt/β-catenin signaling.Journal of bioenergetics and biomembranes · 2021Article
- Kallikrein 11 Down-regulation in Breast Carcinoma: Correlation With Prognostic Parameters.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies have demonstrated that kallikrein-associated peptidase 11 (KLK11) is dysregulated in various cancers. However, the potential roles of KLK11 in esophageal squamous cell carcinoma (ESCC) are still unknown. In our study, we found that the expression of KLK11 in advanced ESCC was significantly down regulated than that in the adjacent tissues, and patients with higher KLK11 expression had markedly increased overall survival rates compared with those with lower KLK11 expression. In addition, up regulation of KLK11 decreased the proliferation capacity of TE-1 and EC18 cells, and down regulation of KLK11 increased the proliferation capacity. To explore the possible mechanism of KLK11 in regulating the proliferation of ESCC, the expression of the related factors in Wnt/β-catenin pathway and cell cycle-mediated factors, such as GSK-3β/p-GSK-3β, β-catenin, Ki67, p-Rb/Rb, CDK6, CDK4 and Cyclin D1, were determined. Furthermore, KLK11 was found to be negatively correlated with the expression of β-catenin in the nucleus, as showed by decreased expression of cyclin D1 and Ki67 through deactivation of the Wnt/β-catenin signaling pathway. XAV-939, a Wnt/β-catenin inhibitor, partially decreased the effects of KLK11 deficiency on ESCC cell proliferation. Finally, we validated that KLK11 inhibited ESCC proliferation
Indexed as
Identifiers
31720087PMC6834484W2984415833What 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.