{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["22(5)"],"submitter":["Li R"],"pubmed_abstract":["The incidence of colorectal cancer (CRC) has remained high in recent years, and 5-fluorouracil (5-FU) is a vital chemotherapeutic agent for its treatment. Our previous study reported that N-myc downstream-regulated gene 4 (NDRG4) plays a tumor-suppressive role in CRC, but the mechanisms associated with NDRG4 and 5-FU chemosensitivity remain unclear. The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3). NDRG4 inhibited the proliferation of CRC cells and the activation of PI3K/AKT and ERK signaling. Furthermore, NDRG4 promoted CRC cell apoptosis induced by 5-FU. Mechanistic analyses revealed that NDRG4 upregulated DDIT3 expression, and that the proapoptotic effect of NDRG4 under 5-FU treatment conditions was dependent on DDIT3. These findings support the biological value of the association between NDRG4, DDIT3 and 5-FU chemosensitivity in CRC, and may advance the clinical treatment of CRC in the future."],"journal":["Oncology letters"],"pagination":["782"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8456512"],"repository":["biostudies-literature"],"pubmed_title":["NDRG4 sensitizes CRC cells to 5-FU by upregulating DDIT3 expression."],"pmcid":["PMC8456512"],"pubmed_authors":["Shen L","Zheng J","He C","Zhang J","Wang S","Feng F","Li R","Shen Y"],"additional_accession":[]},"is_claimable":false,"name":"NDRG4 sensitizes CRC cells to 5-FU by upregulating DDIT3 expression.","description":"The incidence of colorectal cancer (CRC) has remained high in recent years, and 5-fluorouracil (5-FU) is a vital chemotherapeutic agent for its treatment. Our previous study reported that N-myc downstream-regulated gene 4 (NDRG4) plays a tumor-suppressive role in CRC, but the mechanisms associated with NDRG4 and 5-FU chemosensitivity remain unclear. The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3). NDRG4 inhibited the proliferation of CRC cells and the activation of PI3K/AKT and ERK signaling. Furthermore, NDRG4 promoted CRC cell apoptosis induced by 5-FU. Mechanistic analyses revealed that NDRG4 upregulated DDIT3 expression, and that the proapoptotic effect of NDRG4 under 5-FU treatment conditions was dependent on DDIT3. These findings support the biological value of the association between NDRG4, DDIT3 and 5-FU chemosensitivity in CRC, and may advance the clinical treatment of CRC in the future.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2024-11-13T03:11:49.254Z","creation":"2022-02-11T11:38:07.989Z"},"accession":"S-EPMC8456512","cross_references":{"pubmed":["34594423"],"doi":["10.3892/ol.2021.13043"]}}