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Long non‑coding RNA colon cancer‑associated transcript 2 (CCAT2) is dysregulated in a variety of types of human cancer. However, the role of CCAT2 in epithelial ovarian carcinoma (EOC) remains largely unknown. The aim of this study is to investigate the effect of CCAT2 on epithelial‑mesenchymal transition (EMT) and related molecular mechanisms in epithelial ovarian cancer cells. In the current paper, we found that CCAT2 was significantly upregulated in EOC SKOV3, A2780 and HO8910 cell lines compared with the normal ovarian epithelial HUM‑CELL‑0088 cell line. Functional assays demonstrated that the knockdown of CCAT2 inhibited migration and invasion of EOC cells in vitro. Moreover, our results showed that silencing CCAT2 inhibited EMT by the upregulation of epithelial cadherin and downregulation of neural cadherin, zinc finger protein SNAI and Twist‑related protein 1 in SKOV3 and A2780 cell lines. But, that was reversed by the treatment with lithium chloride (LiCl), by which the canonical Wnt/β‑catenin pathway could be activated. In addition, we further investigated the role of CCAT2 in the modulation of Wnt/β‑catenin signaling pathway. Our results revealed that knockdown of CCAT2 inhibited the expression of β‑catenin and the activity of T‑cell factor/lymphoid enhancer factor, acting as a key transcription factor of Wnt signaling pathway. Collectively, these results indicate that CCAT2 may promote EMT, at least partly through Wnt/β‑catenin signaling pathway in EOC cells. Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is a type of hematological malignancy caused by uncontrolled clonal proliferation of hematopoietic stem cells. The special energy metabolism mode of AML relying on oxidative phosphorylation is different from the traditional 'Warburg effect'. However, its mechanism is not clear. In the present study, it was demonstrated that the mRNA expression levels of NADH dehydrogenase subunit 1, 4 and 5 (ND1, ND4 and ND5) were upregulated in AML samples from The Cancer Genome Atlas database using the limma package in the R programming language. Reverse transcription-quantitative PCR and ELISA were used to verify the upregulation of ND1, ND4 and ND5 in clinical samples. Pan-cancer analysis revealed that the expression of ND1 was upregulated only in AML, ND2 was upregulated only in AML and thymoma, and ND4 was upregulated only in AML and kidney chromophobe. In the present study, it was demonstrated that silencing of ND1/4/5 could inhibit the proliferation of AML cells in transplanted tumor of nude mice. Additionally, it was found that oxidative phosphorylation and energy metabolism of AML cells were decreased after silencing of ND1/4/5. In conclusion, the present study suggested that ND1/4/5 may be involved in the regulation of oxidative phosphorylation metabolism in AML as a potential cancer-promoting factor. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is a malignant disease originating from myeloid hematopoietic stem or progenitor cells. It is important to identify molecules associated with the prognosis of AML and conduct an individual risk assessment for different patients. In the present study, the RNA expression profile of 132 patients with AML and 337 healthy individuals were downloaded from the University of California Santa Cruz Xena and the Genotype-Tissue Expression project databases. Differentially expressed mRNA (DEmRNA) transcripts between normal blood and AML blood were identified. Among these, prognosis-associated signature mRNA molecules were screened using univariate Cox and least absolute shrinkage and selection operator regression. A total of four genes, namely, family with sequence similarity 124 member B (FAM124B), 4-hydroxyphenylpyruvate dioxygenase-like protein (HPDL), myeloperoxidase (MPO) and purinergic receptor P2Y1 (P2RY1), were identified using multivariate Cox regression analysis and were used to construct a prognostic scoring system. Moreover, the expression levels of HPDL and MPO were higher in the samples with high immunity scores and estimate scores (sum of stromal score and immune score), compared with those with low scores. Reverse transcription-quantitative PCR and western blot analysis were used to confirm the upregulation of the four candidate genes in AML cell lines as well as in clinical AML samples. In summary, the present study identified a novel mRNA-based prognostic risk scoring system for patients with AML. The four genes used in this scoring system may also play an important role in AML. [ABSTRACT FROM AUTHOR]