Evidence map›Paper›PMID 24988190›Full record

ArticlePloS one2014

Transcutaneous carbon dioxide induces mitochondrial apoptosis and suppresses metastasis of oral squamous cell carcinoma in vivo.

Daisuke Takeda, Takumi Hasegawa, Takeshi Ueha, Yusuke Imai, Akiko Sakakibara, Masaya Minoda, Teruya Kawamoto, Tsutomu Minamikawa, Yasuyuki Shibuya, Toshihiro Akisue and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% 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, 25 citations in OpenAlex.

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  11. Ulinastatin inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling.International journal of clinical and experimental pathology · 2014
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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

13 authors at 2 institutions in 1 country.

Daisuke TakedaDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Takumi HasegawaDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Takeshi UehaNeoChemir, Kobe, Japan.
Yusuke ImaiDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Akiko SakakibaraDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Masaya MinodaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Teruya KawamotoDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Tsutomu MinamikawaDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Yasuyuki ShibuyaDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Toshihiro AkisueDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Yoshitada SakaiDivision of Rehabilitation Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Masahiro KurosakaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Takahide KomoriDepartment of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Kobe University · JPNeoChemir (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Squamous cell carcinoma (SCC) is the main histological type of oral cancer. Its growth rate and incidence of metastasis to regional lymph nodes is influenced by various factors, including hypoxic conditions. We have previously reported that transcutaneous CO2 induces mitochondrial apoptosis and decreases lung metastasis by reoxygenating sarcoma cells. However, previous studies have not determined the sequential mechanism by which transcutaneous CO2 suppresses growth of epithelial tumors, including SCCs. Moreover, there is no report that transcutaneous CO2 suppresses lymphogenous metastasis using human cell lines xenografts. In this study, we examined the effects of transcutaneous CO2 on cancer apoptosis and lymphogenous metastasis using human SCC xenografts. Our results showed that transcutaneous CO2 affects expressions of PGC-1α and TFAM and protein levels of cleavage products of caspase-3, caspase-9 and PARP, which relatives mitochondrial apoptosis. They also showed that transcutaneous CO2 significantly inhibits SCC tumor growth and affects expressions of HIF-1α, VEGF, MMP-2 and MMP-9, which play essential roles in tumor angiogenesis, invasion and metastasis. In conclusion, transcutaneous CO2 suppressed tumor growth, increased mitochondrial apoptosis and decreased the number of lymph node metastasis in human SCC by decreasing intra-tumoral hypoxia and suppressing metastatic potential with no observable effect in vivo. Our findings indicate that transcutaneous CO2 could be a novel therapeutic tool for treating human SCC.

Indexed as

AnimalsApoptosisCarbon DioxideCarcinoma, Squamous CellGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMice, NudeMitochondriaMouth NeoplasmsNeoplasm MetastasisNeoplasm ProteinsXenograft Model Antitumor AssaysCarbon DioxideNeoplasm Proteins

Identifiers

PMID24988190
PMCPMC4079455
OpenAlexW2087218877

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.