ArticleScientific reports2026
TLCD1 correlates with malignant progression of hepatocellular carcinoma and activation of the ERK signaling cascade.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is characterized by high invasiveness and poor prognosis, making the identification of key driver genes crucial for the development of effective treatment strategies. TLCD1 is a member of the TLC domain family, which participates in membrane trafficking and lipid metabolism regulation. While bioinformatics suggests that TLCD1 is abnormally expressed in HCC, experimental evidence for its functions and mechanisms is still lacking. This study aimed to explore the expression pattern, biological functions, and potential molecular mechanism of TLCD1 in HCC. By integrating transcriptome analysis and immunohistochemical detection, it was found that TLCD1 was significantly upregulated in HCC tissues, and its high expression was associated with shortened overall and disease‑free survival in HCC patients. With TLCD1 knockdown and overexpression cell models, CCK‑8, colony formation, wound healing, and transwell assays revealed that overexpression of TLCD1 significantly promoted HCC cell proliferation and metastasis, whereas TLCD1 knockdown exerted an inhibitory effect. Mechanistically, transcriptome data together with western blot analysis indicated that TLCD1 may activate the mitogen‑activated protein kinase (MAPK)/ERK signaling cascade by upregulating the phosphorylation levels of KRAS, ERK1/2, and c‑MYC. In conclusion, TLCD1 may drive the malignant progression of HCC by activating the ERK signaling pathway and may serve as a potential prognostic biomarker and therapeutic target for HCC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.