miR-18a-5p Targets FBP1 to Promote Proliferation, Migration, and Invasion of Liver Cancer Cells and Inhibit Cell Apoptosis

Gao, Shan; Zhu, Dongjie; Zhu, Jianhua; Shen, Lianqiang; Zhu, Ming; Ren, Xuefeng

doi:10.1155/2021/3334065

Cited by 6 publications

(5 citation statements)

References 29 publications

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“…Loss of FBP1 in basal-like breast cancer cells significantly increased glucose uptake, lactate secretion and glycolysis rate, which was conducive to EMT and the maintenance of the basal-like phenotype (17,18). It is also reported that decreased FBP1 expression regulating by miR-18a-5p promotes liver cancer cells migration and invasion (19). Glucose metabolism is a determinant of cancer cell invasion and metastasis.…”

Section: Introductionmentioning

confidence: 92%

Loss of FBP1 by aPKC-ι/Snail Pathway-Mediated Repression Promotes Invasion and Aerobic Glycolysis of Intrahepatic Cholangiocarcinoma

et al. 2021

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Intrahepatic cholangiocarcinoma (ICC) is one of the most commonly diagnosed malignancies worldwide, and the second most common primary liver tumor. The lack of effective diagnostic and treatment methods results in poor patient prognosis and high mortality rate. Atypical protein kinase C-ι (aPKC-ι) is highly expressed in primary and metastatic ICC tissues, and regulates epithelial mesenchymal transition (EMT) through the aPKC-ι/P-Sp1/Snail signaling pathway. Recent studies have correlated aberrant glucose metabolism with EMT. Given the vital role of FBP1 in regulating glucose metabolism in cancer cells, we hypothesized that aPKC-ι downregulates FBP1 in ICC cells through the Snai1 pathway, and enhances glycolysis and metastasis. We confirmed the ability of aPKC-ι promotes glycolysis, invasion and metastasis of cancer cells, and further demonstrated that FBP1 inhibits the malignant properties of ICC cells by antagonizing aPKC-ι. Our findings provide novel insights into the molecular mechanisms of ICC progression and metastasis, as well as a theoretical basis for exploring new treatment strategies.

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Section: Introductionmentioning

confidence: 92%

Loss of FBP1 by aPKC-ι/Snail Pathway-Mediated Repression Promotes Invasion and Aerobic Glycolysis of Intrahepatic Cholangiocarcinoma

et al. 2021

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“…These results indicated that miR−18a-5p acts as an oncogene to participate in OSCC progression and tumorigenesis by regulating the TGF-β1/Smad2 pathway ( 142 ). Also, several studies have shown miR-18a-5p was upregulated in several cancers such as ( 143 , 144 ), hepatocellular carcinoma, prostate cancer and other cancers and can be act as oncomiR by inhibiting apoptosis of cancer cells ( 145 – 147 ). Also, in OSCC cells, miR−18a-5p acts as an oncogene by targeting tumor suppressor genes related to apoptosis.…”

Section: Biogenesis and Function Of Micrornas And Their Roles In Prog...mentioning

confidence: 99%

Non-Coding RNAs and Oral Cancer: Small Molecules With Big Functions

2022

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Oral cancer remains a major public concern with considerable socioeconomic impact in the world. Despite substantial advancements have been made in treating oral cancer, the five-year survival rate for oral cancer remained undesirable, and the molecular mechanisms underlying OSCC carcinogenesis have not been fully understood. Noncoding RNAs (ncRNAs) include transfer RNAs (tRNAs), as well as small RNAs such as microRNAs, and the long ncRNAs such as HOTAIR are a large segment of the transcriptome that do not have apparent protein-coding roles, but they have been verified to play important roles in diverse biological processes, including cancer cell development. Cell death, such as apoptosis, necrosis, and autophagy, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between ncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of oral cancer can be controlled by increasing or decreasing the expression of ncRNAs, a method which confers broad prospects for oral cancer treatment. Therefore, it is urgent for us to understand the influence of ncRNAs on the development of different modes of oral tumor death, and to evaluate whether ncRNAs have the potential to be used as biological targets for inducing cell death and recurrence of chemotherapy. The purpose of this review is to describe the impact of ncRNAs on cell apoptosis and autophagy in oral cancer in order to explore potential targets for oral cancer therapy.

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“…The miRNA miR−18a−5p has already been extensively studied in malignancies and has been shown to act as an onco-miRNA in majority of the cases to facilitate proliferation, migration, and invasion, e.g. liver 14 , prostate 15 , and thyroid cancers 16 . In BC, miR−18a−5p was reported to play an opposing role, where its overexpression hindered migration and invasion 17 .…”

Section: Introductionmentioning

confidence: 99%

MiR-18a-5p attenuates HER2-positive breast cancer development by regulating PI3K/AKT pathway

Liu

Yang

2023

Cancer Biology & Therapy

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Objective: Human epidermal growth factor receptor 2 positive (HER2 + ) breast cancer (BC) is associated with poor prognosis. This study aimed to elucidate the role of miR−18a−5p in regulation of HER2 + -BC progression along with its mechanism of action. Methods: The expression of miR−18a−5p and HER2 in BC cells and tissues was analyzed using quantitative real-time PCR while protein level expression of AKT Serine/Threonine Kinase 1 (AKT), phosphorylated AKT (p-AKT), Phosphatidylinositol 3-kinase (PI3K), phosphorylated-PI3K (p-PI3K), and HER2 were assessed by western blotting. Cell Counting Kit−8, wound healing, and cell adhesion assays were used for in vitro analysis along with xenograft tumor model construction for in vivo analysis. Pearson correlation analysis and dual-luciferase reporter (DLR) assays were used to ascertain the targeting association between miR−18a−5p and HER2. Results: There was a downregulation of miR−18a−5p expression in the BC tissues and cells. Functionally, overexpression of miR−18a−5p prevented BC cells from proliferation, adherence, migration, and activation of the P-PI3K/P-AKT pathway. In vivo experiment revealed that tumor growth was suppressed when miR−18a−5p was overexpressed. In BC, HER2 overexpression increased cell proliferation, cell-cell adhesion, migration, and P-PI3K/P-AKT signaling, but overexpression of miR−18a−5p reversed this effect because of the target relationship between miR−18a−5p and HER2. Conclusion: miR−18a−5p inhibits HER2 + BC progression by targeting HER2 to inhibit PI3K/AKT pathway activation. A theoretical foundation for the identification of new therapeutic targets for HER2 + BC may be provided by the miR−18a−5p – HER2 axis.

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miR-18a-5p Targets FBP1 to Promote Proliferation, Migration, and Invasion of Liver Cancer Cells and Inhibit Cell Apoptosis

Cited by 6 publications

References 29 publications

Loss of FBP1 by aPKC-ι/Snail Pathway-Mediated Repression Promotes Invasion and Aerobic Glycolysis of Intrahepatic Cholangiocarcinoma

Loss of FBP1 by aPKC-ι/Snail Pathway-Mediated Repression Promotes Invasion and Aerobic Glycolysis of Intrahepatic Cholangiocarcinoma

Non-Coding RNAs and Oral Cancer: Small Molecules With Big Functions

MiR-18a-5p attenuates HER2-positive breast cancer development by regulating PI3K/AKT pathway

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