Evidence map›Paper›PMID 26756216›Full record

ArticleOncotarget2016

Lanatoside C suppressed colorectal cancer cell growth by inducing mitochondrial dysfunction and increased radiation sensitivity by impairing DNA damage repair.

Mi Ae Kang, Mi-Sook Kim, Wonwoo Kim, Jee-Hyun Um, Young-Joo Shin, Jie-Young Song, Jae-Hoon Jeong

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Combination ofScientific reports · 2021
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  12. Cytogenotoxic effects ofSaudi journal of biological sciences · 2019
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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

7 authors.

Mi Ae KangResearch Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Mi-Sook KimResearch Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Wonwoo KimResearch Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Jee-Hyun UmKorea Mouse Metabolic Phenotyping Center, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Korea.
Young-Joo ShinDepartment of Radiation Oncology, Inje University Sanggye Paik Hospital, Seoul, Korea.
Jie-Young SongDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Jae-Hoon JeongResearch Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac glycosides are clinically used for cardiac arrhythmias. In this study, we investigated the mechanism responsible for anti-cancer and radiosensitizing effects of lanatoside C in colorectal cancer cells. Lanatoside C-treated cells showed classic patterns of autophagy, which may have been caused by lanatoside C-induced mitochondrial aggregation or degeneration. This mitochondrial dysfunction was due to disruption of K+ homeostasis, possibly through inhibition of Na+/K+-ATPase activity. In addition, lanatoside C sensitized HCT116 cells (but not HT-29 cells) to radiation in vitro. γ-H2AX, a representative marker of DNA damage, were sustained longer after combination of irradiation with lanatoside C, suggesting lanatoside C impaired DNA damage repair processes. Recruitment of 53BP1 to damaged DNA, a critical initiation step for DNA damage repair signaling, was significantly suppressed in lanatoside C-treated HCT116 cells. This may have been due to defects in the RNF8- and RNF168-dependent degradation of KDM4A/JMJD2A that increases 53BP1 recruitment to DNA damage sites. Although lanatoside C alone reduced tumor growth in the mouse xenograft tumor model, combination of lanatoside C and radiation inhibited tumor growth more than single treatments. Thus, lanatoside C could be a potential molecule for anti-cancer drugs and radiosensitizing agents.

Indexed as

AnimalsAutophagyCell Growth ProcessesColorectal NeoplasmsDNA DamageDNA RepairHCT116 CellsHT29 CellsHumansLanatosidesMiceMitochondriaRadiation-Sensitizing AgentsRadiation ToleranceRandom AllocationSignal Transductionlanatoside CLanatosidesRadiation-Sensitizing AgentsautophagyDNA damage repairlanatoside Cmitochondriaradiosensitivity

Identifiers

PMID26756216
PMCPMC4868741

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.