LncRNA FER1L4 induces apoptosis and suppresses EMT and the activation of PI3K/AKT pathway in osteosarcoma cells via inhibiting miR-18a-5p to promote SOCS5

Ye, Fei; Tian, Li; Zhou, Qiang; Feng, Daxiong

doi:10.1016/j.gene.2019.144093

Cited by 51 publications

(37 citation statements)

References 28 publications

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“…As a part of the transcriptome, long-noncoding RNAs (lncRNAs) are involved in various cellular activities by regulating miRNA expression, mRNA stability and processing, as well as protein stability [205]. For example, in osteosarcoma, lncRNA Fer-1-like protein 4 (FER1L4) inhibits miR18a-5p to induce CSCs apoptosis, and suppress the PI3K/Akt pathway and EMT [206]. In CRC, zinc finger E-box-binding homeobox 2 antisense lncRNA (ZEB2-AS1) directly regulates its mRNA to promote ZEB2 translation [207,208].…”

Section: Discussionmentioning

confidence: 99%

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Jiao

Qian

et al. 2019

Cells

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Cancer ranks as the second leading cause of death worldwide, causing a large social and economic burden. However, most anti-cancer treatments face the problems of tumor recurrence and metastasis. Therefore, finding an effective cure for cancer needs to be solved urgently. Recently, the discovery of cancer stem cells (CSCs) provides a new orientation for cancer research and therapy. CSCs share main characteristics with stem cells and are able to generate an entire tumor. Besides, CSCs usually escape from current anti-cancer therapies, which is partly responsible for tumor recurrence and poor prognosis. microRNAs (miRNAs) belong to small noncoding RNA and regulate gene post-transcriptional expression. The dysregulation of miRNAs leads to plenty of diseases, including cancer. The aberrant miRNA expression in CSCs enhances stemness maintenance. In this review, we summarize the role of miRNAs on CSCs in the eight most common cancers, hoping to bridge the research of miRNAs and CSCs with clinical applications. We found that miRNAs can act as tumor promoter or suppressor. The dysregulation of miRNAs enhances cell stemness and contributes to tumor metastasis and therapeutic resistance via the formation of feedback loops and constitutive activation of carcinogenic signaling pathways. More importantly, some miRNAs may be potential targets for diagnosis, prognosis, and cancer treatments.

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Section: Discussionmentioning

confidence: 99%

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Jiao

Qian

et al. 2019

Cells

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“…7a, b). The activity of PI3K/AKT pathway was critical for survival and proliferation of prostate cancer and tightly regulated by FER1L4 in several cancer types [30,31]. Interestingly, in PC-3 and DU145 cells, we also observed that FER1L4 overexpression decreased the phosphorylation of AKT protein which was reversed towards FBXW7 silencing ( Fig.…”

Section: Fer1l4 Suppresses Cell Proliferation and Induce Cell Apoptosmentioning

confidence: 61%

“…Later, several studies suggested that FER1L4 could function as an oncogene or a tumor suppressor in different cancer types [18,[35][36][37]. The most well-characterized role of FER1L4 is its tumor suppressor function as a negative regulator of AKT signaling in cancers [30,31]. Many studies showed that FER1L4 inactivated AKT signaling to suppress cancer progression including osteosarcoma, lung cancer, hepatocellular carcinoma and endometrial carcinoma [28,38,39].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA FER1L4 inhibits prostate cancer progression via sponging miR-92a-3p and upregulation of FBXW7

Huo

Wang

2020

Cancer Cell Int

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Background: Dysregulation of long non-coding RNAs (lncRNAs) is involved in development of prostate cancer. However, the molecular mechanisms of many lncRNAs in prostate cancer have not been studied yet. Methods: The lncRNA Fer-1-like protein 4 (FER1L4) expression was explored in prostate tumors and normal prostate tissues by RT-qPCR and bioinformatic analysis. Overexpression of FER1L4 was performed to evaluate its role in prostate cancer cell proliferation and survival. The molecular mechanism of FER1L4 was investigated by dual luciferase reporter assay, RNA pull down assay, western blotting and RT-qPCR. Results: It was found that FER1L4 was lower in prostate cancer tissues than normal tissues. Higher expression of FER1L4 was associated with prostate cancer tissues of early stage (AJCC stage I/II). Overexpression of FER1L4 inhibited cell proliferation and promoted cell apoptosis in prostate cancer cells. Bioinformatic analysis, RT-qPCR, RNA pull down assay and dual luciferase assay showed that FER1L4 upregulated F-box/WD repeat-containing protein 7 (FBXW7) tumor suppressor via sponging miR-92a-3p. Silencing of FBXW7 reversed the cell phenotypes caused by FER1L4 overexpression in prostate cancer cells. Conclusion: The data demonstrated that FER1L4, a downregulated lncRNA in prostate cancer, was pivotal for cell proliferation and survival of prostate cancer. The study provided new sights into understanding of the signaling network in prostate cancer and implied that FER1L4 might be a biomarker for patients with prostate cancer.

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“…Several transcription factors also take part in the regulation of EMT, including the Snail/Slug family, Twist, and SIP1/ZEB2, function as molecular switches for the EMT program [33][34][35]. Recent studies have shown that dysregulated expression of lncRNAs in some cancers may regulate EMT and affect disease progression [36]. Here we identi ed LincHOXA10, A novel lncRNA, drives the EMT of CRC cells though TGF-β1/SMADs pathway.…”

Section: Discussionmentioning

confidence: 90%

LincHOXA10 Facilitates Colorectal Cancer Development By Regulating HOXA10-Mediated Epithelial-Mesenchymal Transtion

Zhu

Zhang

et al. 2020

Preprint

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Background: Long non-coding RNAs (lncRNAs) have been reported to play an important role in tumorigenesis and metastasis of human colorectal cancer (CRC). However, the specific role of LincHOXA10 in CRC remains unknown.Methods: The expression of LincHOXA10 and HOXA10 in CRC cells and tissue samples was measured by quantitative reverse transcription PCR (qRT-PCR). The protein expression of HOXA10, E-cadherin, N-cadherin, Vinmentin, p-smad2 and p-smad3 was assessed by Western blotting or immunofluorescence staining. Cell proliferation, migration, and invasion were assessed by the MTT and transwell assays. Tumor growth in vivo was carried out by subcutaneous tumor formation in nude mice.Results: In the present study, we found that LincHOXA10 expression was significantly higher in human CRC tissues than the paired normal tissues. In fact, LincHOXA10 level correlated with the CRC tumor sizes and lymphatic metastasis. In cultured CRC cells, knockdown of LincHOXA10 inhibited cell proliferation, migration and invasion. LincHOXA10 deficiency also attenuated CRC tumor growth in vivo. Mechanistically, LincHOXA10 interacted with HOXA10 and regulated its expression. HOXA10 levels were interrelated to the LincHOXA10 level in CRC cells. Functionally, HOXA10 was essential for TGF-β1/SMADs-induced epithelial -mesenchymal transition of CRC cells, and HOXA10 played a critical role in mediating the function of LincHOXA10. Importantly, HOXA10 expression was significantly up-regulated in human CRC tissues.Conclusions: LincHOXA10 facilitates CRC development and metastasis via regulating HOXA10-mediated epithelial-mesenchymal transition of CRC cells.

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LncRNA FER1L4 induces apoptosis and suppresses EMT and the activation of PI3K/AKT pathway in osteosarcoma cells via inhibiting miR-18a-5p to promote SOCS5

Cited by 51 publications

References 28 publications

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Long non-coding RNA FER1L4 inhibits prostate cancer progression via sponging miR-92a-3p and upregulation of FBXW7

LincHOXA10 Facilitates Colorectal Cancer Development By Regulating HOXA10-Mediated Epithelial-Mesenchymal Transtion

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