ArticleJournal of gastrointestinal oncology2021
Increased BST-2 expression by HBV infection promotes HBV-associated HCC tumorigenesis.
Article in Journal of gastrointestinal oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- NF-κB signaling in hepatocellular carcinoma: Mechanisms of tumor progression, immune evasion, and therapeutic resistance.Translational oncology · 2026Review
- Review
- Exploration of the Prognostic Markers of Multiple Myeloma Based on Cuproptosis-Related Genes.Cancer reports (Hoboken, N.J.) · 2025Article
- The endoplasmic reticulum degradation-enhancing α-mannosidase-like protein 3 attenuates the unfolded protein response and has pro-survival and pro-viral roles in hepatoma cells and hepatocellular carcinoma patients.Journal of biomedical science · 2025Article
- Bone marrow stromal cell antigen 2: Tumor biology, signaling pathway and therapeutic targeting (Review).Oncology reports · 2024Review
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
backgroundThe majority of hepatocellular carcinoma (HCC) is closely associated with hepatitis B virus (HBV) infection, while the mechanism of HCC induced by HBV is debatable. Bone marrow stromal cell antigen 2 (BST-2), an N-glycoprotein, has been characterized as an oncogenic factor in several types of cancer. However, whether BST-2 plays an important role in HCC tumorigenesis remains unknown.
methodsA total of 182 HCC tumorous and adjacent nontumor liver tissues were collected. HepG2, Huh7, L02, HepAD38, and HEK293T cell lines were adopted in this study. Tumor proliferation was detected by CCK8, transwell, wound healing, colony formation assays
resultsHere, we observed the higher BST-2 expression in HBV-infected HCC than their paired adjacent tissues and HBV-uninfected HCC tissues, particularly more aberrant non-N-glycosylated BST-2 in HBV-infected HCC tumors. We also observed the increased ER degradation-enhancing α-mannosidase-like protein 3 (EDEM3), which is trimming of N-linked glycans by sequential removal of mannose residues, might result in more non-N-glycosylated form of BST-2. Moreover, we demonstrated that BST-2 and non-N-glycosylated BST-2 N65/92A mutant, not only enhanced the tumor characteristics of hepatoma cell lines
conclusionsOur findings illuminate the novel function of BST-2 as an oncogene of HBV-associated HCC, and highlight the novel relationship of N-glycosylation of BST-2 in regulating HCC tumorigenesis
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.