Evidence map›Paper›PMID 37553596›Full record

ArticleCell & bioscience2023

KITENIN promotes aerobic glycolysis through PKM2 induction by upregulating the c-Myc/hnRNPs axis in colorectal cancer.

Mücahit Varlı, Sung Jin Kim, Myung-Giun Noh, Yoon Gyoon Kim, Hyung-Ho Ha, Kyung Keun Kim, Hangun Kim

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-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

14 citing papers in PubMed, 14 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

7 authors at 3 institutions in 1 country.

Mücahit VarlıCollege of Pharmacy, Sunchon National University, 255 Jungang-ro, Sunchon, Jeonnam, 57922, Republic of Korea.ORCID http://orcid.org/0000-0001-6175-4015
Sung Jin KimCollege of Pharmacy, Sunchon National University, 255 Jungang-ro, Sunchon, Jeonnam, 57922, Republic of Korea.
Myung-Giun NohDepartment of Pathology, Chonnam National University Medical School, 160 Baekseoro, Dong-gu, Gwanju, 61469, Republic of Korea.
Yoon Gyoon KimCollege of Pharmacy, Dankook University, 119 Dandaero, Dongnam-gu, 31116, Cheonan-si, Republic of Korea.
Hyung-Ho HaCollege of Pharmacy, Sunchon National University, 255 Jungang-ro, Sunchon, Jeonnam, 57922, Republic of Korea.
Kyung Keun KimDepartment of Pharmacology, Chonnam National University Medical School, 160 Baekseoro, Dong-gu, Gwangju, 61469, Republic of Korea.ORCID http://orcid.org/0000-0002-7346-9526
Hangun KimCollege of Pharmacy, Sunchon National University, 255 Jungang-ro, Sunchon, Jeonnam, 57922, Republic of Korea. hangunkim@sunchon.ac.kr.ORCID http://orcid.org/0000-0001-5889-8907
Chonnam National University · KRSunchon National University · KRDankook University · KR

Funding

National Research Foundation of Korea NRF-2021M3E5E7022123
6 · The paper itself

Abstract

purposeThe oncoprotein KAI1 C-terminal interacting tetraspanin (KITENIN; vang-like 1) promotes cell metastasis, invasion, and angiogenesis, resulting in shorter survival times in cancer patients. Here, we aimed to determine the effects of KITENIN on the energy metabolism of human colorectal cancer cells. EXPERIMENTAL

designThe effects of KITENIN on energy metabolism were evaluated using in vitro assays. The GEPIA web tool was used to extrapolate the clinical relevance of KITENIN in cancer cell metabolism. The bioavailability and effect of the disintegrator of KITENIN complex compounds were evaluated by LC-MS, in vivo animal assay.

resultsKITENIN markedly upregulated the glycolytic proton efflux rate and aerobic glycolysis by increasing the expression of GLUT1, HK2, PKM2, and LDHA. β-catenin, CD44, CyclinD1 and HIF-1A, including c-Myc, were upregulated by KITENIN expression. In addition, KITENIN promoted nuclear PKM2 and PKM2-induced transactivation, which in turn, increased the expression of downstream mediators. This was found to be mediated through an effect of c-Myc on the transcription of hnRNP isoforms and a switch to the M2 isoform of pyruvate kinase, which increased aerobic glycolysis. The disintegration of KITENIN complex by silencing the KITENIN or MYO1D downregulated aerobic glycolysis. The disintegrator of KITENIN complex compound DKC1125 and its optimized form, DKC-C14S, exhibited the inhibition activity of KITENIN-mediated aerobic glycolysis in vitro and in vivo.

conclusionsThe oncoprotein KITENIN induces PKM2-mediated aerobic glycolysis by upregulating the c-Myc/hnRNPs axis.

Indexed as

Aerobic glycolysisc-MycColorectal cancerDisintegrator of KITENIN complex compoundsErbB4hnRNPKITENINMYO1DPKM2Transcriptional regulator

Identifiers

PMID37553596
PMCPMC10410973
OpenAlexW4385658266

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.