Wild-type IDH1 Knockout Leads to G0/G1 Arrest, Impairs Cancer Cell Proliferation, Altering Glycolysis, and the TCA Cycle in Colon Cancer

Basit Öğe Kaydı
dc.authorid0000-0002-1615-0535tr
dc.contributor.authorEsra BULUT ATALAY
dc.contributor.authorŞERİF ŞENTÜRK
dc.contributor.authorHÜLYA AYAR KAYALI
dc.date.accessioned2024-03-05T08:38:56Z
dc.date.available2024-03-05T08:38:56Z
dc.date.issued12/01/2023tr
dc.departmentFen Bilimleri Enstitüsütr
dc.description.abstractThe isocitrate dehydrogenase (IDH), which participates in the TCA cycle, is an important key enzyme in regulating cell metabolism. The effect of the metabolic IDH enzyme on cancer pathogenesis has recently been shown in different types of cancer. However, the role of wild-type (wt) IDH1 in the development of colon cancer is still unknown. Our study investigated the role of the IDH1 enzyme in key hallmarks of colon cancer using various methods such as wound healing, cell cycle, colony formation ability, invasion, and apoptosis analysis. Furthermore, cell metabolism was investigated by pyruvate analysis, dinitrosalicylic acid, and HPLC methods. In addition, CRISPR/Cas9 tool was utilized to knockout the IDH1 gene in colon adenocarcinoma cells (SW620). Further studies were performed in two isogenic IDH1 KO clones. Our findings in both clones suggest that IDH1 KO results in G0/ G1 arrest, and reduces proliferation by approximately twofold compared to IDH1 WT cells. In addition, the invasion, migration, and colony formation abilities of IDH1 KO clones were significantly decreased accompanied by significant morphological changes. In the context of metabolism, intracellular glucose, pyruvate, αKG, and malate levels were decreased, while the intracellular citrate level was increased in IDH1 KO clones as compared to IDH1 WT cells. Our results reveal that wt IDH1 knockout leads to a decrease in the aggressive features of colon cancer cells. In conclusion, we reported that wt IDH1 has an effective role in colon cancer progression and could be a potential therapeutic target.tr
dc.description.sponsorshipyoktr
dc.identifier.urihttps://hdl.handle.net/20.500.12418/14661
dc.language.isoenen_US
dc.publisherSpringertr
dc.relation.ispartofBiochemical Geneticsen_US
dc.relation.publicationcategoryUluslararası Editör Denetimli Dergide Makaletr
dc.rightsinfo:eu-repo/semantics/openAccesstr
dc.subjectColon cancer · Glycolysis · Knockout · TCA cycle · Wild-type IDH1 · IDH1 silencing · CRISPR/Cas9 method · Metabolism · Therapeutic targettr
dc.titleWild-type IDH1 Knockout Leads to G0/G1 Arrest, Impairs Cancer Cell Proliferation, Altering Glycolysis, and the TCA Cycle in Colon Canceren_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
Küçük Resim
İsim:
Wild‑type IDH1 Knockout Leads to G0-G1 Arrest, Impairs Cancer Cell Proliferation, Altering Glycolysis, and the TCA cycle.pdf
Boyut:
1.56 MB
Biçim:
Adobe Portable Document Format
Açıklama:
İndir
Lisans paketi
Listeleniyor 1 - 1 / 1
Küçük Resim Yok
İsim:
license.txt
Boyut:
1.44 KB
Biçim:
Item-specific license agreed upon to submission
Açıklama:
İndir

Koleksiyon

Biyokimya Bölümü Koleksiyonu