<scp>FBXW</scp>7 modulates malignant potential and cisplatin‐induced apoptosis in cholangiocarcinoma through <scp>NOTCH</scp>1 and <scp>MCL</scp>1

Mori, Akiko; Masuda, Koichi; Ohtsuka, Hideo; Shijo, Masahiro; Ariake, Kyohei; Fukase, Koji; Sakata, Naoaki; Mizuma, Masamichi; Morikawa, Takanori; Hayashi, Hiroki; Nakagawa, Kazuhiko; Motoi, Fuyuhiko; Naitoh, Takeshi; Fujishima, Fumiyoshi; Unno, Michiaki

doi:10.1111/cas.13829

Cited by 15 publications

(9 citation statements)

References 51 publications

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“…Recently studies have suggested that aberrant activation of the Notch signaling accelerates cell proliferation in endometrial cancer, and suppression of mTOR signaling pathway in EC inhibits tumor initiation and progression [45,46]. Mori et al demonstrated that FBXW7 modulates cell apoptosis via inhibiting Notch signaling pathway [47]. Our results also showed that over-expressing FBXW7 suppressed Notch signaling related protein and p-mTOR/mTOR, and regulated the proliferation and apoptosis of EC cells through Notch/mTOR signaling pathway.…”

Section: Discussionsupporting

confidence: 71%

STYX/FBXW7 axis participates in the development of endometrial cancer cell via Notch–mTOR signaling pathway

et al. 2020

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Endometrial cancer (EC) is the most common gynecologic malignancy in world. It has been reported that the mutation rate of FBXW7 is frequent in EC, but the specific functions of FBXW7 remain unknown in EC. In the present study, we revealed the role and mechanism of FBXW7 in EC cells. Compared with adjacent nontumor tissues, the FBXW7 expression level was lower in EC tissues. However, the level of STYX was in contrast with the expression of FBXW7 in EC tissues. And STYX interacted with FBXW7 and then down-regulated its expression level in EC. Over-expression of FBXW7 inhibited cell proliferation and facilitated apoptosis in EC cells, whereas silencing FBXW7 acted an opposite effect on EC cells. And the process of FBXW7 participated the proliferation and apoptosis in EC was regulated by STYX. FBXW7 suppressed the expression of Notch pathway related protein, and further inhibited the phosphorylation of mTOR. In addition, we also found that mTOR activitor (MHY1485) and Notch activator (Jagged-1) reversed the effect of over-expressing FBXW7 on cell proliferation and cell apoptosis. And Notch inhibitor (DAPT) counteracted the impact of over-expressing STYX on cell proliferation and cell apoptosis. Collectively, the present study verified that STYX inhibited the expression level of FBXW7 in EC, and then promoted cell proliferation but suppressed apoptosis through Notch–mTOR signaling pathway, which promoted carcinogenesis and progression of EC.

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Section: Discussionsupporting

confidence: 71%

STYX/FBXW7 axis participates in the development of endometrial cancer cell via Notch–mTOR signaling pathway

et al. 2020

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“…As a member of the F-box protein family, FBXW7 is an important tumor-suppressor gene and one of the most-commonly deregulated ubiquitin-proteasome system proteins in human cancers [12]. The degradation of oncoproteins, such as cyclin E, c-Myc, Mcl-1, mTOR, Jun, Notch, and AURKA, can be regulated by FBXW7 [29,30]. As a frequently-mutated gene in cancers, we identified that FBXW7 was downregulated in HCC specimens compared with that of normal tissues.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA hsa_circ_0001306 Functions as a Competing Endogenous RNA to Regulate FBXW7 Expression by Sponging miR-527 in Hepatocellular Carcinoma

Fan

Zhao

et al. 2021

J. Cancer

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Hepatocellular carcinoma (HCC) is one of the most common types of cancer worldwide. Circular RNAs (circRNAs) have been reported to regulate many types of cancers, including HCC. The purpose of this study was to investigate the potential roles of hsa_circ_0001306 in HCC. Firstly, the downregulation of hsa_circ_0001306 was identified by high-throughput RNA sequencing and further verified by qRT-PCR. Secondly, we evaluated the effects of hsa_circ_0001306 on HCC cell proliferation, invasion, cell cycle. Finally, we used an animal model to validate the in vitro experimental results. The expression of hsa_circ_0001306 was closely related to tumor size. Knockdown of hsa_circ_0001306 could downregulate F-box and WD repeat domain containing 7(FBXW7), a target of miR-527, thereby promoting HCC cell proliferation and invasion. Furthermore, hsa_circ_0001306 siRNA increased the multiplication rate of HCC tumors. Mechanistic studies indicated that hsa_circ_0001306 acts as a ceRNA for miR-527, which resulted in the reduction of its endogenous target, FBXW7. Hsa_circ_001306 is significantly downregulated in HCC, and the hsa_circ_0001306/miR-527/FBXW7 axis plays an important role in HCC progression.

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“…For instance, FBXW7 restrains the epithelial-to-mesenchymal transition (EMT) process in non-small-cell lung cancer (30). FBXW7 inhibits cholangiocarcinoma progression via NOTCH1 and MCL1 (31). In the present study, the FBXW7 gene was shown to be a downstream target gene of miR-5000-3p in laryngocarcinoma.…”

Section: Discussionmentioning

confidence: 55%

E2F6-Mediated Downregulation of MIR22HG Facilitates the Progression of Laryngocarcinoma by Targeting the miR-5000-3p/FBXW7 Axis

Chen

Ali

Ruben

et al. 2020

Molecular and Cellular Biology

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Recently, abundant evidence has clarified that long noncoding RNAs (lncRNAs) play an oncogenic or anticancer role in the tumorigenesis and development of diverse human cancers. Described as a crucial regulator in some cancers, MIR22HG has not yet been studied in laryngocarcinoma and therefore the underlying regulatory role of MIR22HG in laryngocarcinoma is worth detecting. In this study, MIR22HG expression in laryngocarcinoma cells was confirmed to be downregulated, and upregulated MIR22HG expression led to suppressive effects on laryngocarcinoma cell proliferation and migration. Molecular mechanism assays revealed that MIR22HG sponges miR-5000-3p in laryngocarcinoma cells. Besides, decreased expression of miR-5000-3p suppressed laryngocarcinoma cell proliferation and migration. Moreover, the FBXW7 gene was reported to be a downstream target gene of miR-5000-3p in laryngocarcinoma cells. More importantly, rescue assays verified that FBXW7 depletion or miR-5000-3p upregulation countervailed the repressive effects of MIR22HG overexpression on laryngocarcinoma progression. In addition, E2F6 was proved to be capable of inhibiting MIR22HG transcription in laryngocarcinoma cells. To sum up, E2F6-induced downregulation of MIR22HG promotes laryngocarcinoma progression through the miR-5000-3p/FBXW7 axis.

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FBXW7 modulates malignant potential and cisplatin‐induced apoptosis in cholangiocarcinoma through NOTCH1 and MCL1

Cited by 15 publications

References 51 publications

STYX/FBXW7 axis participates in the development of endometrial cancer cell via Notch–mTOR signaling pathway

STYX/FBXW7 axis participates in the development of endometrial cancer cell via Notch–mTOR signaling pathway

Circular RNA hsa_circ_0001306 Functions as a Competing Endogenous RNA to Regulate FBXW7 Expression by Sponging miR-527 in Hepatocellular Carcinoma

E2F6-Mediated Downregulation of MIR22HG Facilitates the Progression of Laryngocarcinoma by Targeting the miR-5000-3p/FBXW7 Axis

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