Evidence map›Paper›PMID 25629974›Full record

ArticlePloS one2015

Modulation of intracellular calcium levels by calcium lactate affects colon cancer cell motility through calcium-dependent calpain.

Pasupathi Sundaramoorthy, Jae Jun Sim, Yeong-Su Jang, Siddhartha Kumar Mishra, Keun-Yeong Jeong, Poonam Mander, Oh Byung Chul, Won-Sik Shim, Seung Hyun Oh, Ky-Youb Nam and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 32 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

11 authors at 2 institutions in 2 countries.

Pasupathi SundaramoorthyGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Jae Jun SimGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Yeong-Su JangGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Siddhartha Kumar MishraGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea; Department of Zoology, School of Biological Sciences, Dr. Harisingh Gour Central University, Sagar 470003, India.
Keun-Yeong JeongGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Poonam ManderGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Oh Byung ChulGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea; Lee Gil Ya Cancer and Diabetes Institute, Department of Molecular Medicine, Gachon University, Inchon 406-840, Republic of Korea.
Won-Sik ShimGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Seung Hyun OhGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Ky-Youb NamGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Hwan Mook KimGachon Institute of Pharmaceutical Sciences, Gachon University, Incheon 406-840, Republic of Korea.
Gachon University · KRDr. Hari Singh Gour University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cell motility is a key phenomenon regulating invasion and metastasis. Focal adhesion kinase (FAK) plays a major role in cellular adhesion and metastasis of various cancers. The relationship between dietary supplementation of calcium and colon cancer has been extensively investigated. However, the effect of calcium (Ca2+) supplementation on calpain-FAK-motility is not clearly understood. We sought to identify the mechanism of FAK cleavage through Ca2+ bound lactate (CaLa), its downstream signaling and role in the motility of human colon cancer cells. We found that treating HCT116 and HT-29 cells with CaLa immediately increased the intracellular Ca2+ (iCa2+) levels for a prolonged period of time. Ca2+ influx induced cleavage of FAK into an N-terminal FAK (FERM domain) in a dose-dependent manner. Phosphorylated FAK (p-FAK) was also cleaved in to its p-N-terminal FAK. CaLa increased colon cancer cells motility. Calpeptin, a calpain inhibitor, reversed the effects of CaLa on FAK and pFAK cleavage in both cancer cell lines. The cleaved FAK translocates into the nucleus and modulates p53 stability through MDM2-associated ubiquitination. CaLa-induced Ca2+ influx increased the motility of colon cancer cells was mediated by calpain activity through FAK and pFAK protein destabilization. In conclusion, these results suggest that careful consideration may be given in deciding dietary Ca2+ supplementation to patient undergoing treatment for metastatic cancer.

Indexed as

CalciumCalcium CompoundsCalpainCell AdhesionCell LineCell MovementColonic NeoplasmsFocal Adhesion Protein-Tyrosine KinasesHT29 CellsHumansLactatesPhosphorylationSignal TransductionWound HealingCalciumCalcium Compoundscalcium lactateCalpainFocal Adhesion Protein-Tyrosine KinasesLactates

Identifiers

PMID25629974
PMCPMC4309579
OpenAlexW1977012174

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.