Knock-down of PSAT1 Enhances Sensitivity of NSCLC Cells to Glutamine-limiting Conditions.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Dec 2019
Historique:
received: 11 11 2019
revised: 16 11 2019
accepted: 18 11 2019
entrez: 8 12 2019
pubmed: 8 12 2019
medline: 18 12 2019
Statut: ppublish

Résumé

Phosphoserine aminotransferase 1 (PSAT1) is an enzyme implicated in serine biosynthesis, and its overexpression has been linked to cancer cell proliferation. Therefore, targeting PSAT1 is considered to be an anticancer strategy. The viability of non-small cell lung cancer (NSCLC) cells was measured by MTT assay. Protein and mRNA expression were determined by western blot and reverse transcription polymerase chain reaction, respectively. Glutamine-limiting conditions were generated through glutamine deprivation or CB-839 treatment, which induced PSAT1 expression in NSCLC cells. PSAT1 expression induced by glutamine-limiting conditions was regulated by activating transcription factor 4. Knock-down of PSAT1 enhanced the sensitivity of NSCLC cells to glutamine-limiting conditions. Interestingly, ionizing radiation induced PSAT1 expression, and knocking down PSAT1 increased cell sensitivity to ionizing radiation. Inhibiting PSAT1 might aid in the treatment of lung cancer, and PSAT1 may be a therapeutic target for lung cancer.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
Phosphoserine aminotransferase 1 (PSAT1) is an enzyme implicated in serine biosynthesis, and its overexpression has been linked to cancer cell proliferation. Therefore, targeting PSAT1 is considered to be an anticancer strategy.
MATERIALS AND METHODS METHODS
The viability of non-small cell lung cancer (NSCLC) cells was measured by MTT assay. Protein and mRNA expression were determined by western blot and reverse transcription polymerase chain reaction, respectively.
RESULTS RESULTS
Glutamine-limiting conditions were generated through glutamine deprivation or CB-839 treatment, which induced PSAT1 expression in NSCLC cells. PSAT1 expression induced by glutamine-limiting conditions was regulated by activating transcription factor 4. Knock-down of PSAT1 enhanced the sensitivity of NSCLC cells to glutamine-limiting conditions. Interestingly, ionizing radiation induced PSAT1 expression, and knocking down PSAT1 increased cell sensitivity to ionizing radiation.
CONCLUSION CONCLUSIONS
Inhibiting PSAT1 might aid in the treatment of lung cancer, and PSAT1 may be a therapeutic target for lung cancer.

Identifiants

pubmed: 31810937
pii: 39/12/6723
doi: 10.21873/anticanres.13887
doi:

Substances chimiques

ATF4 protein, human 0
Benzeneacetamides 0
CB-839 0
RNA, Messenger 0
Thiadiazoles 0
Glutamine 0RH81L854J
Activating Transcription Factor 4 145891-90-3
Transaminases EC 2.6.1.-
phosphoserine aminotransferase EC 2.6.1.52
Glutaminase EC 3.5.1.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

6723-6730

Informations de copyright

Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Hyeon-Ok Jin (HO)

KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea hyeonok@kirams.re.kr parkic@kirams.re.kr.

Sung-Eun Hong (SE)

Division of Fusion Radiology Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Ji-Young Kim (JY)

KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Se-Kyeong Jang (SK)

Division of Fusion Radiology Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Young-Sun Kim (YS)

KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Ju-Hee Sim (JH)

KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Ac-Chin Oh (AC)

Department of Laboratory Medicine, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Heyjin Kim (H)

Department of Laboratory Medicine, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Young Jun Hong (YJ)

Department of Laboratory Medicine, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Jin-Kyung Lee (JK)

KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Department of Laboratory Medicine, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

In-Chul Park (IC)

Division of Fusion Radiology Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea hyeonok@kirams.re.kr parkic@kirams.re.kr.

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Classifications MeSH