ArticleCell communication and signaling : CCS2025
Lycorine hydrochloride inhibits cholangiocarcinoma through cholesterol biosynthesis and PTPN11 nuclear translocation.
Article in Cell communication and signaling : CCS, 2025. 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
9 authors.
Funding
Abstract
backgroundIntrahepatic Cholangiocarcinoma (ICC) is a highly aggressive malignancy with limited treatment options. Identifying novel therapeutic agents for ICC is crucial. Numerous natural compounds have demonstrated remarkable anti-tumor activities and can enhance the efficacy of chemotherapy. Thus, our study aimed to screen natural compounds for their anti-ICC effects.
methodsA total of 640 natural compounds were screened using a cell viability assay to identify potential compounds that could inhibit the proliferation of ICC cells. The anti-ICC effects of Lycorine Hydrochloride (LY) were confirmed through cell proliferation, colony formation, cell cycle, migration, and invasion assays, as well as in xenograft models. Bioinformatics analyses and validation experiments (Quantitative real-time PCR, Western blot, and immunostaining assays) were utilized to investigate the roles of genes (SQLE, FDFT1, and PTPN11) in ICC. RNA sequencing and immunofluorescence staining were performed to elucidate underlying molecular mechanisms.
resultsLY was identified as a potential ICC inhibitor, exhibiting anti-ICC effects both in vitro and in vivo. Mechanistically, LY inhibited cholesterol synthesis in tumor cells by down-regulating the expression of SQLE and FDFT1. The knockdown of SQLE or FDFT1 significantly inhibited ICC cell proliferation and colony formation. RNA sequencing confirmed that inhibition of FDFT1 suppressed the cholesterol biosynthesis pathway, while SQLE inhibition affected specific oncogenic pathways. Additionally, immunofluorescence staining revealed that down-regulation of SQLE reduced PTPN11 expression and inhibited its nuclear translocation. Furthermore, pharmacological inhibition of SQLE and FDFT1 by LY significantly enhanced sensitivity to several common chemotherapeutic drugs for ICC. Notably, the combination of LY and Gemcitabine (GEM) displayed the most potent synergistic anti-tumor effect across various tumor types.
conclusionThese findings identify Lycorine Hydrochloride as a promising treatment alternative for ICC and propose a novel combination strategy (LY + GEM) for treating multiple solid tumors.
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.