MiR-155-5p inhibits PDK1 and promotes autophagy via the mTOR pathway in cervical cancer

Wang, Fang; Shu, Shan; Huo, Yan; Xie, Zipeng; Fang, Yehong; Qi, Zhiying; Chen, Fengzhen; Li, Yongmei; Sun, Bei

doi:10.1016/j.biocel.2018.04.005

Cited by 72 publications

(44 citation statements)

References 24 publications

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“…miR‐155‐5p is a multifunctional miRNA, which can regulate the pathophysiological processes, such as inflammation, angiocardiopathy, and carcinogenesis . miR‐155 can suppress the progression of gastric cancer and promote autophagy via the mTOR pathway in cervical cancer . In lung cancer cells, miR‐155‐5p can suppress the migration and invasion of cancer cells via targeting Smad2 .…”

Section: Discussionmentioning

confidence: 89%

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

et al. 2019

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MicroRNAs (miRNAs) play important roles in tumorigenesis of various cancers. Recent study suggested that miRNAs are involved in the therapeutic functions of radiation during cancer treatment. We found that radiation can decrease the migration and invasion of non-small cell lung cancer (NSCLC) cells. Mechanistically, radiation can significantly increase the expression of miR-155-5p and miR-760 in NSCLC cells. Knockdown of miR-155-5p and miR-760 can attenuate radiation suppressed proliferation of NSCLC cells. Among the various targets of miR-155-5p, radiation can decrease the expression of HIF-1α. Similarly, radiation can also suppress the expression of IL-6 via a miR-760 dependent pathway. Gain and loss of function studies confirmed that both HIF-1α and IL-6 were involved in the radiation suppressed proliferation of NSCLC cells. Collectively, our data showed that radiation can regulate the expression of miR-155-5p and miR-760 to suppress the malignancy of NSCLC cells. © 2019 BioFactors, 45(3):393-400, 2019

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Section: Discussionmentioning

confidence: 89%

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

et al. 2019

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“…Dysregulation of this process contributes to tumor progression [13]. Autophagy, which is lower in cancerous than in normal cells, has been observed in malignant cells and cells with malignant potential [72]. An evaluation of the levels of miR155 in cervical and nasopharyngeal cancer shows that if members of the mTOR pathway (RHEB, RICTOR and RPS6KB2) are activated, the levels of miR155 are lowered and autophagy is decreased.…”

Section: Hypoxic Modulation Of Carcinogenesis Via Mtor Signalingmentioning

confidence: 99%

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

Sobočan

Bračič

Knez

et al. 2020

Cancers

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Studies of the mechanistic (mammalian) target of rapamycin inhibitors (mTOR) represent a step towards the targeted treatment of gynecological cancers. It has been shown that women with increased levels of mTOR signaling pathway targets have worse prognosis compared to women with normal mTOR levels. Yet, targeting mTOR alone has led to unsatisfactory outcomes in gynecological cancer. The aim of our review was therefore to provide an overview of the most recent clinical results and basic findings on the interplay of mTOR signaling and cold shock proteins in gynecological malignancies. Due to their oncogenic activity, there are promising data showing that mTOR and Y-box-protein 1 (YB-1) dual targeting improves the inhibition of carcinogenic activity. Although several components differentially expressed in patients with ovarian, endometrial, and cervical cancer of the mTOR were identified, there are only a few investigated downstream actors in gynecological cancer connecting them with YB-1. Our analysis shows that YB-1 is an important player impacting AKT as well as the downstream actors interacting with mTOR such as epidermal growth factor receptor (EGFR), Snail or E-cadherin.

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“…Recently, the involvement of miRNAs in tumorigenesis and their signi cance as effective biomarkers are also becoming increasingly appreciated [14]. miR-155-5p has been found to regulate the development of various cancer types, including human epithelial ovarian cancer [16], cervical cancer [17,18], and colon cancer [19]. It has been reported that some certain long non-coding RNAs (lncRNAs) suppress HCC development by sponging miR-155-5p [20]; miR-155-5p modulated the malignancy of HCC by regulating Wnt/β-catenin signaling or suppressing PTEN through the PI3K/Akt pathway [21,22]; therefore, miR-155-5p can be a promising therapeutic target for HCC patients.…”

Section: Discussionmentioning

confidence: 99%

CircTP63 Promotes Hepatocellular Carcinoma Progression by Sponging miR-155-5p and Upregulating ZBTB18

Wang

Che

2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is the leading cause of tumor-related death worldwide due to high morbidity and mortality, yet still lacking biomarkers and therapies. Circular RNAs (circRNAs) are a group of non-coding RNAs that regulate gene expression through interacting with miRNAs, implicating in the tumorigenesis and progression. A novel circRNA, circTP63, was reported to be an oncogene in HCC. However, its role in HCC remains unclear.Methods: qRT-PCR was used to assess the mRNA levels of CircTP63 in 90 pairs of tumor and adjacent normal tissues from HCC patients, one human normal hepatic epithelial cell line and HCC cell lines. CCK-8, colony formation, transwell, and flow cytometry assays were performed to detect the cellular function of circTP63/miR-155-5p/ZBTB18 in HCC cells. Bioinformatic analysis, RNA pull-down and luciferase assays were used to determine the interaction among circTP63/miR-155-5p/ZBTB18. Results: circTP63 was significantly upregulated in HCC tissues and cell lines. High circTP63 expression is closely associated with the tumor stages, lymph node metastasis, and poor prognosis of HCC patients. Functionally, knockdown of circTP63 inhibited cell proliferation, migration, invasion, and promoted cell apoptosis of HCC. Meanwhile, overexpression of circTP63 enhanced HCC progression. Mechanically, circTP63 was a sponge of miR-155-5p to facilitate the ZBTB18 expression, and the ZBTB18 expression in HCC tissues was negatively associated with the survival rate of HCC patients. Furthermore, the reduced tumor-promoting effect on HCC cells induced by knockdown of circTP63 can be reversed by miR-155-5p inhibitor or ZBTB18 overexpression. Conclusion: Our data highlight a critical circTP63-miR-155-5p-ZBTB18 regulatory network involved in the HCC progression, gaining mechanistic insights into the function of CircRNAs in HCC progression, and providing effective biomarkers and therapeutic targets for HCC treatment.

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MiR-155-5p inhibits PDK1 and promotes autophagy via the mTOR pathway in cervical cancer

Cited by 72 publications

References 24 publications

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

The Communication between the PI3K/AKT/mTOR Pathway and Y-Box Binding Protein-1 in Gynecological Cancer

CircTP63 Promotes Hepatocellular Carcinoma Progression by Sponging miR-155-5p and Upregulating ZBTB18

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