Evidence map›Paper›PMID 27923905›Full record

ArticleIntegrative cancer therapies2017

β-Lapachone Inhibits Lung Metastasis of Colorectal Cancer by Inducing Apoptosis of CT26 Cells.

Ji-Ye Kee, Yo-Han Han, Jinbong Park, Dae-Seung Kim, Jeong-Geon Mun, Kwang Seok Ahn, Hyun-Jung Kim, Jae-Young Um, Seung-Heon Hong

Open access · goldAbstract read
In one paragraph

Article in Integrative cancer therapies, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  10. Vimentin as a target for the treatment of COVID-19.BMJ open respiratory research · 2020
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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

9 authors at 3 institutions in 1 country.

Ji-Ye Kee1 Wonkwang University, Iksan, Republic of Korea.
Yo-Han Han1 Wonkwang University, Iksan, Republic of Korea.
Jinbong Park2 Kyung Hee University, Seoul, Republic of Korea.
Dae-Seung Kim1 Wonkwang University, Iksan, Republic of Korea.
Jeong-Geon Mun1 Wonkwang University, Iksan, Republic of Korea.
Kwang Seok Ahn2 Kyung Hee University, Seoul, Republic of Korea.
Hyun-Jung Kim3 Dong-eui Institute of Technology, Busan, Republic of Korea.
Jae-Young Um2 Kyung Hee University, Seoul, Republic of Korea.
Seung-Heon Hong1 Wonkwang University, Iksan, Republic of Korea.
Wonkwang University · KRKyung Hee University · KRDong-Eui University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundβ-Lapachone is a quinone-containing compound found in red lapacho ( Tabebuia impetiginosa, syn. T avellanedae) trees. Lapacho has been used in traditional medicine by several South and Central American indigenous people to treat various types of cancer. The purpose of this study was to investigate the antimetastatic properties of β-lapachone and the underlying mechanisms using colon cancer cells.

methodsThis research used metastatic murine colon cancer cell lines, colon 26 (CT26) and colon 38 (MC38). A WST assay, annexin V assay, cell cycle analysis, wound healing assay, invasion assay, western blot analysis, and real-time reverse transcription-polymerase chain reaction were performed to examine the effects of β-lapachone on metastatic phenotypes and molecular mechanisms. The effect of β-lapachone on lung metastasis was assessed in a mouse experimental metastasis model.

resultsWe found that the inhibition of proliferation of the colon cancer cell lines by β-lapachone was due to the induction of apoptosis and cell cycle arrest. β-Lapachone induced the apoptosis of CT26 cells through caspase-3, -8, and -9 activation; poly(ADP-ribose) polymerase cleavage; and downregulation of the Bcl-2 family in a dose- and time-dependent manner. In addition, a low concentration of β-lapachone decreased the cell migration and invasion by decreasing the expression of matrix metalloproteinases-2 and -9, and increased the expression of tissue inhibitors of metalloproteinases-1 and -2. Moreover, β-lapachone treatment regulated the expression of epithelial-mesenchymal transition markers such as E- and N-cadherin, vimentin, β-catenin, and Snail in CT26 cells. In the mouse experimental metastasis model, β-lapachone significantly inhibited the lung metastasis of CT26 cells.

conclusionsOur results demonstrated the inhibitory effect of β-lapachone on colorectal lung metastasis. This compound may be useful for developing therapeutic agents to treat metastatic cancer.

Indexed as

AnimalsApoptosisBiomarkers, TumorCaspasesCell Cycle CheckpointsCell Line, TumorCell ProliferationColorectal NeoplasmsDown-RegulationEpithelial-Mesenchymal TransitionFemaleLung NeoplasmsMiceMice, Inbred BALB CNaphthoquinonesProto-Oncogene Proteins c-bcl-2beta-lapachoneBiomarkers, TumorCaspasesNaphthoquinonesProto-Oncogene Proteins c-bcl-2apoptosiscolorectal cancerCT26 cellslung metastasisβ-lapachone

Identifiers

PMID27923905
PMCPMC5739146
OpenAlexW2560313907

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Registered trials

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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.