MicroRNA‑454‑3p inhibits cell proliferation and invasion in esophageal cancer by targeting insulin‑like growth factor 2 mRNA‑binding protein 1

Yan, Aiting; Wang, Cuizhu; Zheng, Liangfeng; Zhou, Jian; Zhang, Yan

doi:10.3892/ol.2020.12223

Cited by 13 publications

(18 citation statements)

References 35 publications

(39 reference statements)

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“…In addition, low miR-454-3p expression in bladder cancer tissues, predicted poor prognosis of bladder cancer patients ( 14 ). Moreover, miR-454-3p functioned as a tumor inhibitor of esophageal cancer by inhibiting the ERK/AKT signaling pathways ( 35 ). With regard to NSCLC, the expression of miR-454-3p was downregulated in NSCLC tissues and cell lines ( 13 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑454‑3p inhibits non‑small cell lung cancer cell proliferation and metastasis by targeting TGFB2

Liao

Liang

Kang³

et al. 2021

Oncol Rep

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Accumulating studies have suggested that microRNAs (miRs) play a significant role in lung cancer development and progression, especially in non-small cell lung cancer (NSCLC). The present study aimed to investigate the associations between miR-454-3p and NSCLC progression. qPCR assay was applied to examine the expression of miR-454-3p and transforming growth factor-β2 (TGFB2) in tissues and cell lines. CCK-8 and EdU assays were used to detect cell proliferation. Wound-healing and Transwell assays were conducted to assess cell migration and invasion. Western blotting assay was performed to explore the protein levels of epithelial-mesenchymal transition (EMT) markers. The interaction between miR-454-3p and TGFB2 was investigated with a luciferase reporter assay. miR-454-3p was downregulated in NSCLC tissues and NSCLC cell lines. miR-454-3p overexpression led to the suppression of proliferation, migration, and invasion in A549 and NCI-H1650 cells. In addition, the overexpression of miR-454-3p in A549 and NCI-H1650 cells significantly inhibited EMT. TGFB2 was revealed to be a direct target of miR-454-3p by using TargetScan database and luciferase reporter assay. TGFB2 was observed to be upregulated in NSCLC tissues and cell lines. Further mechanistic studies revealed that the inhibitory effects of miR-454-3p on NSCLC were reversed upon overexpression of TGFB2. These findings provided strong evidence that miR-454-3p suppressed NSCLC cell proliferation and metastasis by targeting TGFB2. The study suggests that targeting miR-454-3p could be a promising strategy for treating NSCLC.

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Section: Discussionmentioning

confidence: 99%

miR‑454‑3p inhibits non‑small cell lung cancer cell proliferation and metastasis by targeting TGFB2

Liao

Liang

Kang³

et al. 2021

Oncol Rep

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“…Although many of the cancer-related mRNA targets of IGF2BP1 were found to promote cell proliferation, migration and invasion [32,33,44], several were shown to take part in indirect suppression of tumor growth and metastasis [45,46]. We found that IGF2BP1 is required for gemcitabine resistance, and that RRP9 interacts with IGF2BP1, leading to reduced apoptosis and increased growth in PC cells.…”

Section: Discussionmentioning

confidence: 86%

RRP9 Promotes Gemcitabine Resistance in Pancreatic Cancer Via Activating AKT Signaling Pathway

Zhang

Yao

et al. 2022

Preprint

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BackgroundPancreatic cancer (PC) is a highly lethal malignancy regarding digestive system, which is the fourth leading factor of cancer-related mortalities in the globe. Prognosis is poor due to diagnosis at advanced disease stage, low rates of surgical resection, and resistance to traditional radiotherapy and chemotherapy. In order to develop novel therapeutic strategies, further elucidation of the molecular mechanisms underlying PC chemoresistance is required. Ribosomal RNA biogenesis has been implicated in tumorigenesis. Small nucleolar RNAs (snoRNAs) is responsible for post-transcriptional modifications of ribosomal RNAs during biogenesis, which have been identified as potential markers of various cancers. Here, we investigate the U3 snoRNA-associated protein RRP9/U3-55K along with its role in the development of PC and gemcitabine resistance.MethodsqRT-PCR, western blot and immunohistochemical staining assays were employed to detect RRP9 expression in human PC tissue samples and cell lines. RRP9-overexpression and siRNA-RRP9 plasmids were constructed to test the effects of RRP9 overexpression and knockdown on cell viability investigated by MTT assay, colony formation, and apoptosis measured by FACS and western blot assays. Immunoprecipitation, immunofluorescence staining and luciferase assays were utilized to demonstrate a relationship between RRP9 and IGF2BP1. A subcutaneous xenograft tumor model was elucidated in BALB/c nude mice to examine the RRP9 role in PC in vivo.ResultsSignificantly elevated RRP9 expression was observed in PC tissues than normal tissues, which was negatively correlated with patient prognosis. We found that RRP9 promoted gemcitabine resistance in PC in vivo and in vitro. Mechanistically, RRP9 activated AKT signaling pathway through interacting with DNA binding region of IGF2BP1 in PC cells, thereby promoting PC progression, and inducing gemcitabine resistance through a reduction in DNA damage and inhibition of apoptosis. Treatment with a combination of the AKT inhibitor MK-2206 and gemcitabine significantly inhibited tumor proliferation induced by overexpression of RRP9 in vitro and in vivo.ConclusionsOur data reveal that RRP9 has a critical function to induce gemcitabine chemoresistance in PC through the IGF2BP1/AKT signaling pathway activation, which might be a candidate to sensitize PC cells to gemcitabine.

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“…In contrast, inhibition of miR-454-3p up-regulated PTEN expression, but attenuated the phosphorylation of AKT and mTOR, resulting in resensitization to oxaliplatin. Notably, previous studies reported that miR-454-3p inhibited AKT signaling pathway by targeting insulinlike growth factor 2 mRNA-binding protein 1 (IGF2BP1) in esophageal cancer (ESCA) ( 35 ) and targeting c-met in nasopharyngeal carcinoma ( 36 ), resulting in the suppression of cell growth and enhancement of cisplatin sensitivity. These inconsistent results may indicate that the role of miR-454-3p in modulating tumor progression and chemotherapeutic sensitivity was dependent on the types of human malignancies.…”

Section: Discussionmentioning

confidence: 99%

MiR-454-3p Promotes Oxaliplatin Resistance by Targeting PTEN in Colorectal Cancer

et al. 2021

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Colorectal cancer is one of the most common malignancies worldwide. Oxaliplatin is the first-line chemotherapeutic agent for the treatment of advanced colorectal cancer. However, acquired resistance to oxaliplatin limits its therapeutic efficacy, and the underlying mechanism remains largely unclear. In this study, we compared the expression of a panel of microRNAs (miRNAs) between oxaliplatin-sensitive and -resistant HCT-116 colorectal cancer cells. We found that miR-454-3p was significantly up-regulated in oxaliplatin-resistant cells and was the most differently expressed miRNA. Interestingly, we observed that inhibition of miR-454-3p resensitized resistant cells to oxaliplatin and enhanced oxaliplatin-induced cellular apoptosis. Moreover, we determined that miR-454-3p promoted oxaliplatin resistance through targeting PTEN and activating the AKT signaling pathway. In vivo study revealed that overexpression of miR-454-3p decreased the sensitivity of HCT-116 xenograft tumors to oxaliplatin treatment in a mouse model. Clinically, overexpression of miR-454-3p was associated with decreased responsiveness to oxaliplatin-based chemotherapy, as well as a short progression-free survival. Taken together, our study indicated that the expression of miR-454-3p could be used to predict oxaliplatin sensitivity, and targeting miR-454-3p could overcome oxaliplatin resistance in colorectal cancer.

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MicroRNA‑454‑3p inhibits cell proliferation and invasion in esophageal cancer by targeting insulin‑like growth factor 2 mRNA‑binding protein 1

Cited by 13 publications

References 35 publications

miR‑454‑3p inhibits non‑small cell lung cancer cell proliferation and metastasis by targeting TGFB2

miR‑454‑3p inhibits non‑small cell lung cancer cell proliferation and metastasis by targeting TGFB2

RRP9 Promotes Gemcitabine Resistance in Pancreatic Cancer Via Activating AKT Signaling Pathway

MiR-454-3p Promotes Oxaliplatin Resistance by Targeting PTEN in Colorectal Cancer

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