Evidence map›Paper›PMID 36899823›Full record

ArticleCells2023

Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity.

Fumimasa Tomooka, Kosuke Kaji, Norihisa Nishimura, Takahiro Kubo, Satoshi Iwai, Akihiko Shibamoto, Junya Suzuki, Koh Kitagawa, Tadashi Namisaki, Takemi Akahane and 2 more

Open access · goldFull text read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Fumimasa TomookaDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Kosuke KajiDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Norihisa NishimuraDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.ORCID 0000-0002-6295-3283
Takahiro KuboDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Satoshi IwaiDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.ORCID 0000-0003-3575-5609
Akihiko ShibamotoDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Junya SuzukiDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Koh KitagawaDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.ORCID 0000-0001-5794-1512
Tadashi NamisakiDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.ORCID 0000-0002-3158-5318
Takemi AkahaneDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.ORCID 0000-0002-6675-0475
Akira MitoroDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Hitoshi YoshijiDepartment of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Nara Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intrahepatic cholangiocarcinoma (iCCA), the second most common primary liver cancer, has high mortality rates because of its limited treatment options and acquired resistance to chemotherapy. Sulforaphane (SFN), a naturally occurring organosulfur compound found in cruciferous vegetables, exhibits multiple therapeutic properties, such as histone deacetylase (HDAC) inhibition and anti-cancer effects. This study assessed the effects of the combination of SFN and gemcitabine (GEM) on human iCCA cell growth. HuCCT-1 and HuH28 cells, representing moderately differentiated and undifferentiated iCCA, respectively, were treated with SFN and/or GEM. SFN concentration dependently reduced total HDAC activity and promoted total histone H3 acetylation in both iCCA cell lines. SFN synergistically augmented the GEM-mediated attenuation of cell viability and proliferation by inducing G2/M cell cycle arrest and apoptosis in both cell lines, as indicated by the cleavage of caspase-3. SFN also inhibited cancer cell invasion and decreased the expression of pro-angiogenic markers (VEGFA, VEGFR2, HIF-1α, and eNOS) in both iCCA cell lines. Notably, SFN effectively inhibited the GEM-mediated induction of epithelial-mesenchymal transition (EMT). A xenograft assay demonstrated that SFN and GEM substantially attenuated human iCCA cell-derived tumor growth with decreased Ki67

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaAnimalsApoptosisBile Ducts, IntrahepaticCell Line, TumorG2 Phase Cell Cycle CheckpointsGemcitabineHumansIsothiocyanatesMiceSulfoxidesGemcitabineIsothiocyanatessulforaphaneSulfoxidesangiogenesisapoptosiscell cycle arrestchemoresistanceEMT

Identifiers

PMID36899823
PMCPMC10000472
OpenAlexW4321496399

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read46
Read underepoch 390

Registered trials

None linked

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.