miR-144 inhibits the IGF1R-ERK1/2 signaling pathway via NUDCD1 to suppress the proliferation and metastasis of colorectal cancer cells: a study based on bioinformatics and in vitro and in vivo verification

Han, Bin; Xu, Ke; Feng, Dan; Bai, Yang; Liu, Yangqi; Zhang, Yuanyuan; Zhou, Liming

doi:10.1007/s00432-022-03951-0

Cited by 7 publications

(6 citation statements)

References 58 publications

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“…Previous research reported the biological implications of NUDCD1 in other cancer types. For instance, loss of NUDCD1 mitigates the proliferation and metastases of pancreatic cancer ( 47 ) and colorectal cancer ( 48 ) through the epithelial-mesenchymal transition (EMT) process for non-small cell lung cancer cells through activating IGF1R - ERK1/2 ( 49 ). GPX4 , a member of the GSH peroxidase family, reduces lipid peroxidase in cells, thereby aiding in cell survival ( 50 ).…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis-related genes with post-transcriptional regulation mechanisms in hepatocellular carcinoma determined by bioinformatics and experimental validation

Zhu¹,

Cheng²,

Feng³

et al. 2022

Ann Transl Med

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Background: Ferroptosis is a form of iron-dependent cell death with increased free iron and massive lipid peroxidation. The discovery of ferroptosis offers insights into hepatocellular carcinoma (HCC) treatment.However, post-transcriptional regulation mechanisms of ferroptosis in HCC remain to be elucidated. The present study explored ferroptosis-related genes and their post-transcriptional regulation mechanisms in HCC.Methods: A ferroptosis score was computed in The Cancer Genome Atlas (TCGA) cohort via gene set variation analysis (GSVA), and ferroptosis-related genes were screened by differential expression and correlation analyses. CircRNA/miRNA-mediated ferroptosis-related genes were predicted, and associations of ferroptosis-related genes with m 1 A/m 5 C/m 6 A regulators were analyzed. Immune cell infiltrations were inferred via CIBERSORT. NUDCD1 expression was examined in L-02, SMMC7721, and HepG2 cells via real time quantitative polymerase chain reaction (RT-qPCR) and western blots. After NUDCD1 was silenced, cell viability, glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1) expression, and oxidized glutathione/glutathione (GSSG/GSH) and glutathione (GSH) levels were detected in SMMC7721 and HepG2 cells. Results:The ferroptosis score was linked to poor overall survival (OS) of HCC, which was independent of other clinicopathological parameters. Ten ferroptosis-related genes were determined, namely UGT1A6, ATP6V1C1, MAFG, NUDCD1, PPP1R1A, TSKU, CTSB, AIFM2, CTSA, and CTNND2, which were post-transcriptionally regulated by circRNA/miRNA and m 1 A/m 5 C/m 6 A modifications in HCC. Most were significantly linked with most immune cell compositions within the immune microenvironment, and contributed to undesirable clinical outcomes. NUDCD1 was up-regulated in HCC cells, and its loss facilitated the ferroptosis of HCC cells.Conclusions: Overall, our findings determined ferroptosis-related genes post-transcriptionally regulated by circRNA/miRNA and m 1 A/m 5 C/m 6 A RNA modifications, and experiments demonstrated that loss of

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Section: Discussionmentioning

confidence: 99%

Ferroptosis-related genes with post-transcriptional regulation mechanisms in hepatocellular carcinoma determined by bioinformatics and experimental validation

Zhu¹,

Cheng²,

Feng³

et al. 2022

Ann Transl Med

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“…P < 0.05 was considered statistically significant. Statistical analysis was performed as described previously [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

ELFN1-AS1 promotes GDF15-mediated immune escape of colorectal cancer from NK cells by facilitating GCN5 and SND1 association

Han

Chen

et al. 2023

Discov Onc

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The ability of colorectal cancer (CRC) cells to escape from natural killer (NK) cell immune surveillance leads to anti-tumor treatment failure. The long non-coding RNA (lncRNA) ELFN1-AS1 is aberrantly expressed in multiple tumors suggesting a role as an oncogene in cancer development. However, whether ELFN1-AS1 regulates immune surveillance in CRC is unclear. Here, we determined that ELFN1-AS1 enhanced the ability of CRC cells to escape from NK cell surveillance in vitro and in vivo. In addition, we confirmed that ELFN1-AS1 in CRC cells attenuated the activity of NK cell by down-regulating NKG2D and GZMB via the GDF15/JNK pathway. Furthermore, mechanistic investigations demonstrated that ELFN1-AS1 enhanced the interaction between the GCN5 and SND1 protein and this influenced H3k9ac enrichment at the GDF15 promotor to stimulate GDF15 production in CRC cells. Taken together, our findings indicate that ELFN1-AS1 in CRC cells suppresses NK cell cytotoxicity and ELFN1-AS1 is a potential therapeutic target for CRC.

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“…Flow cytometry of propidium iodide (PI)‐stained cells was used for cell cycle measurements, and the FACS plot was analyzed by ModFit3.2. Annexin V‐FITC/PI double staining was used to detect apoptosis based on previous descriptions 19 . Oxaliplatin treatment of cell lines was performed using a single 10 μM dosage overnight.…”

Section: Methodsmentioning

confidence: 99%

“…Annexin V-FITC/PI double staining was used to detect apoptosis based on previous descriptions. 19 Oxaliplatin treatment of cell lines was performed using a single 10 μM dosage overnight. /well) and cultured for 24 h. The operations were conducted to Co-IP Kits (P2179M; Beyotime) in accordance with the instructions.…”

Section: Cell Cycle Apoptosis Detection and Oxaliplatin Treatmentmentioning

confidence: 99%

SUMO2/3 promotes the progression and oxaliplatin resistance of colorectal cancer through facilitating the SUMOylation at Ku80‐K307

Feng

Yuan

et al. 2023

BioFactors

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Colorectal cancer (CRC) is one of the most prevalent cancers worldwide and is typically treated with the FOLFOX regimen (folinic acid, 5‐fluorouracil, and oxaliplatin). However, oxaliplatin resistance remains a serious clinical problem. In the present study, we found that SUMO2/3 was overexpressed in CRC tissues and exogenous overexpression of SUMO2/3 promoted CRC cell proliferation, extension, and invasion and positively regulated the cell cycle. In contrast, SUMO2/3 gene knockdowns inhibited migration and repressed cell viability in vitro and in vivo. In addition, we found that SUMO2/3 was recruited to the cell nucleus and suppressed oxaliplatin‐induced apoptosis of CRC cells. Moreover, Ku80, a DNA‐binding protein essential for the repair of DNA double‐strand breaks, was confirmed to bind with SUMO2/3. Notably, Ku80 undergoes SUMOylation at K307 by SUMO2/3 and this correlated with apoptosis in CRC cells suffering oxaliplatin stress. Collectively, we found that SUMO2/3 plays a specific role in CRC tumorigenesis and acts through Ku80 SUMOylation which is linked with the development of CRC‐oxaliplatin resistance.

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miR-144 inhibits the IGF1R-ERK1/2 signaling pathway via NUDCD1 to suppress the proliferation and metastasis of colorectal cancer cells: a study based on bioinformatics and in vitro and in vivo verification

Cited by 7 publications

References 58 publications

Ferroptosis-related genes with post-transcriptional regulation mechanisms in hepatocellular carcinoma determined by bioinformatics and experimental validation

Ferroptosis-related genes with post-transcriptional regulation mechanisms in hepatocellular carcinoma determined by bioinformatics and experimental validation

ELFN1-AS1 promotes GDF15-mediated immune escape of colorectal cancer from NK cells by facilitating GCN5 and SND1 association

SUMO2/3 promotes the progression and oxaliplatin resistance of colorectal cancer through facilitating the SUMOylation at Ku80‐K307

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