Combination Treatment of OSI-906 with Aurora B Inhibitor Reduces Cell Viability via Cyclin B1 Degradation-Induced Mitotic Slippage

Ikeda, Yuki; Yasutake, Ryuji; Yuki, Ryuzaburo; Saito, Youhei; Nakayama, Yuji

doi:10.3390/ijms22115706

Cited by 5 publications

(2 citation statements)

References 51 publications

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“…Long non‐coding RNAs (lncRNAs), a kind of non‐coding RNAs (ncRNAs), comprise no less than 200 nucleotides mostly without protein‐encoding function. Several lncRNAs have been found to control the progression of NSCL‐CSCs, such as lncRNA OIP5‐AS1 could confer the CSC‐traits of NSCLC via directly interacting with Oct4 mRNA, a critical master regulator of CSC, and thus enhancing Oct4 mRNA stability and expression 4 ; LncRNA PKMYT1AR facilitates CSC maintenance in NSCLC by activating the Wnt signaling pathway. Additionally, the sponge type of TUSC7 regulation on miR‐146a suppressed the CSC's renewal in Erlotinib resistant PC9 cells 5 .…”

Section: Introductionmentioning

confidence: 99%

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Long non‐coding RNA TDRG1 aggravates lung cancer stemness by binding to Sox2mRNA

Lü

Cheng

Mao

et al. 2022

Environmental Toxicology

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The roles of long non-coding RNA TDRG1 have been revealed in several tumors, especially its roles in CSC progression have been recently elucidated; However, its effects in lung CSC progression have not been revealed. In the present study, we collected 3D non-adherent spheres as the CSC model to measure lncRNA TDRG1 level in lung CSC and the parental lung cancer cells, and found that TDRG1 level was significantly upregulated in lung CSCs compared to that of parental lung cancer cells.Then we constructed the lung CSCs with or without TDRG1 stable knockdown and lung cancer cells with or without TDRG1 stable overexpression. It was found that TDRG1 positively regulated lung cancer stemness. Mechanistically, we identified that TDRG1 directly bound to Sox2 mRNA, which is a critical stemness regulator, enhanced its mRNA stability, and thus increased Sox2 expression. Indeed, we demonstrated that TDRG1 aggravated lung cancer stemness dependent on Sox2 expression.

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Section: Introductionmentioning

confidence: 99%

“…You Lu and Jing Cheng contributed to this work equally. mRNA, a critical master regulator of CSC, and thus enhancing Oct4 mRNA stability and expression 4 ; LncRNA PKMYT1AR facilitates CSC maintenance in NSCLC by activating the Wnt signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA TDRG1 aggravates lung cancer stemness by binding to Sox2mRNA

Lü

Cheng

Mao

et al. 2022

Environmental Toxicology

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MEOX1 suppresses the progression of lung cancer cells by inhibiting the cell‐cycle checkpoint gene CCNB1

Xie

Rui

et al. 2021

Environmental Toxicology

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The previous study has shown that transcriptional factor MEOX1 could promote proliferation and sphere formation ability of non‐small cell lung cancer (NSCLC) cells, however, we found that MEOX1 mRNA was lowly expressed in lung cancer tissues compared to that in normal adjacent tissues, and MEOX1 mRNA expression was positively correlated with the survival of lung cancer patients, especially in lung adenocarcinoma patients. Functional experiments using in vitro and in vivo experiments revealed that stable overexpression of MEOX1 significantly suppressed the proliferation ability, promoted cell cycle arrest in G2 phase, and apoptotic ability of NSCLC cells. Additionally, it was identified that MEOX1 and CCNB1 mRNA expression exhibited a negative correlation in different lung cancer tissues. Mechanistically, we indicated that MEOX1 bound to the transcriptional initiation site of CCNB1 and thus suppressed CCNB1 expression. Notably, CCNB1 overexpression rescued the inhibition of MEOX1 overexpression on NSCLC progression. This study deciphers a novel MEOX1/CCNB1 axis suppressing NSCLC progression.

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Construction of a novel lipid drop-mitochondria-associated genetic profile for predicting the survival and prognosis of lung adenocarcinoma

Cai,

Lin,

Cheng

et al. 2024

Discov Onc

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Background Lung adenocarcinoma (LUAD) is one of the most common malignant tumors. Although several treatments have been proposed, the long-term prognosis of this cancer is poor. Lipid droplets and mitochondria are important organelles that regulate energy metabolism in cells and are postulated to promote the occurrence and progression of tumors. However, few risk prediction models have been constructed based on lipid drop-mitochondria-related genes (LMRGs). Methods In this study, we constructed a lipid drop-mitochondrial (LD-M) risk score model based on data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Biological functions and clinical benefits associated with the various risk scores were analyzed using R software, GraphPad Prism 9, and the online database system. Results An LD-M risk score model comprising ABLIM3, AK4, CAV2, CPS1, CYP24A1, DLGAP5, FGR, and SH3BP5, was developed and its predictive power was validated. The risk score was closely associated with the cell cycle. Immunophenoscore (IPS) and Tumor immune dysfunction and exclusion (TIDE) results demonstrated that the low-risk group was more sensitive to immunotherapy. Drug sensitivity analysis indicated that BMS-754807, ZM447439, SB216763, and other drugs had lower IC50 values in the low-risk group. Conclusion Our results suggest that the LD-M risk score is an effective prognostic indicator for individualized treatment of LUAD.

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Combination Treatment of OSI-906 with Aurora B Inhibitor Reduces Cell Viability via Cyclin B1 Degradation-Induced Mitotic Slippage

Cited by 5 publications

References 51 publications

Long non‐coding RNA TDRG1 aggravates lung cancer stemness by binding to Sox2mRNA

Long non‐coding RNA TDRG1 aggravates lung cancer stemness by binding to Sox2mRNA

MEOX1 suppresses the progression of lung cancer cells by inhibiting the cell‐cycle checkpoint gene CCNB1

Construction of a novel lipid drop-mitochondria-associated genetic profile for predicting the survival and prognosis of lung adenocarcinoma

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