miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2

Sep 22, 2026

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Metabolic reprogramming is essential in hepatocarcinogenesis, yet the drivers in primary liver cancer remain unclear. This study identified differentially expressed microRNAs between primary liver cancer and normal tissues, then validated miR-10b-5p and SLC38A2 expression by RT-qPCR, IHC, and WB. Cellular proliferation, migration, invasion, and apoptosis were measured with CCK-8, Transwell, flow cytometry, and TUNEL assays. Dual-luciferase testing confirmed miR-10b-5p targeting SLC38A2, and a BALB/c nude-mouse xenograft model assessed tumorigenicity. Untargeted LC-MS metabolomics characterized in vivo metabolic shifts, showing miR-10b-5p promotes tumor growth and worsens metabolic reprogramming through SLC38A2, supporting diagnostic and therapeutic potential.

LanguageEnglish

CategoryResearch & Report

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Pages15

Reading Time38 min

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Introduction

Metabolic reprogramming in primary liver cancer

MicroRNAs and metabolic regulation

RESEARCH PAPER miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2 Mingzhi Xiaa, Jie Chenb, Yingyun Huc, Bin Qud, Qianqian Bud, and Haoming Shen d aBreast Surgery Department I, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, P.R. China; bLiver and gallbladder surgery Department I, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, P.R. China; cHunan Cancer Prevention and Control Office, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, P.R. China; dDepartment of Clinical Laboratory, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, P.R. China ABSTRACT Metabolic reprogramming plays a critical role in hepatocarcinogenesis. However, the mechanisms regulating metabolic reprogramming in primary liver cancer (PLC) are unknown. Differentially expressed miRNAs between PLC and normal tissues were identified using bioinformatic analysis. RT-qPCR was used to determine miR-10b-5p and SCL38A2 expression levels. IHC, WB, and TUNEL assays were used to assess the proliferation and apoptosis of the tissues. The proliferation, migration, invasion, and apoptosis of PLC cells were determined using the CCK-8 assay, Transwell assay, and flow cytometry. The interaction between miR-10b-5p and SLC38A2 was determined using dual-luciferase reporter assay. A PLC xenograft model in BALB/c nude mice was established, and tumorigenicity and SLC38A2 expression were estimated. Finally, liquid chromatography – mass spectrometry (LC-MS) untargeted metabolomics was used to analyze the metabolic profiles of xenograft PLC tissues in nude mice. miR-10b-5p was a key molecule in the regulation of PLC. Compared with para-carcinoma tissues, miR-10b-5p expression was increased in tumor tissues. miR-10b-5p facilitated proliferation, migration, and invasion of PLC cells. Mechanistically, miR-10b-5p targeted SLC38A2 to promote PLC tumor growth. Additionally, miR-10b-5p altered the metabolic features of PLC in vivo. Overexpression of miR-10b-5p resulted in remarkably higher amounts of lumichrome, folic acid, octanoylcarnitine, and Beta-Nicotinamide adenine dinucleotide, but lower levels of 2-methylpropanal, glycyl-leucine, and 2-hydroxycaproic acid. miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment. ARTICLE HISTORY Received 2 April 2023 Revised 28 June 2023 Accepted 4 February 2024 KEYWORDS Primary liver cancer; tumorigenicity; SLC38A2; metabolic reprogramming 1. Introduction Primary liver cancer (PLC), the seventh most prevalent cancer, is the second leading cause of cancer-related mortality globally. 1 PLC includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC), and other types of liver cancer, accounting for approximately 80%, 15%, and 5%, respectively.2 Due to the limited accuracy of biomarkers for early diagnosis and prognosis, the majority of PLCs are found at an advanced stage and lack effective therapeutic options, resulting in a high death rate.3 The liver is an essential metabolic regulator in the body, coordinating toxin removal; regulating glucose, lipid, and amino acid metabolism; and sustaining metabolic homeostasis.4 By modifying metabolic patterns, tumor cells adapt to the microenvironment of hypoxia and nutrient deprivation and proliferate rapidly. This biological process is known as metabolic reprogramming, and is regarded as an important hallmark of cancers.5 Currently, no effective therapeutic strategies for PLC metabolism are available in the clinic.6

FAQs

Why are miR-10b-5p and SLC38A2 considered potential clinical targets?

miR-10b-5p is increased in tumor tissues and promotes tumorigenic phenotypes by targeting SLC38A2, and its presence aligns with measurable metabolic reprogramming patterns relevant to diagnosis and treatment.

Sep 22, 2026

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