F‐box protein <scp>FBXL</scp>2 inhibits gastric cancer proliferation by ubiquitin‐mediated degradation of forkhead box M1

Li, Liangqing; Pan, Dun; Chen, Hui; Zhang, Lin; Xie, Weihao

doi:10.1002/1873-3468.12071

Cited by 28 publications

(17 citation statements)

References 25 publications

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“…It also inhibited leukemic cell proliferation by targeting cyclin D2 (31). FBXL2 also decreased gastric cancer proliferation by promoting degradation of forkhead box M1 (32).…”

Section: Discussionmentioning

confidence: 96%

miRNA-346 promotes proliferation, migration and invasion in liver cancer

Xia

Duan

et al. 2017

Oncology Letters

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Abstract. Liver cancer primarily accounts for the majority of malignancies of the liver. MicroRNAs (miRNAs) are endogenous non-coding RNAs, which are important in tumorigenesis. Abnormal expression of microRNA-346 (miR-346) has been demonstrated in various types of human cancer, however, its expression and potential molecular mechanism in liver cancer remains to be elucidated. Expression levels of miR-346 in liver cancer cell lines were determined by quantitative polymerase chain reaction. The effect of miR-346 on proliferation was evaluated by an MTT assay; cell migration and invasion were evaluated by Transwell migration and invasion assays and target protein expression was determined by western blotting. The present study observed that miR-346 was upregulated in liver cancer cell lines. miR-346 overexpression promoted cell proliferation, migration and invasion in liver cancer cells and conversely, inhibition of miR-346 resulted in the opposite effects. Furthermore, F-Box and leucine rich repeat protein (FBXL)2 was identified as a direct target of miR-346. miR-346 promoted proliferation, migration and invasion of liver cancer via FBXL2. Overall, these findings demonstrated that miR-346 may act as a potential prognostic marker and therapeutic target against liver cancer in the future.

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“…It also inhibited leukemic cell proliferation by targeting cyclin D2 (31). FBXL2 also decreased gastric cancer proliferation by promoting degradation of forkhead box M1 (32).…”

Section: Discussionmentioning

confidence: 96%

miRNA-346 promotes proliferation, migration and invasion in liver cancer

Xia

Duan

et al. 2017

Oncology Letters

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“…21 Besides, FBXL2 inhibits gastric cancer proliferation and invasion by ubiquitin-mediated degradation of forkhead box M1 (FoxM1) transcription factor in gastric cancer cells. 22 Chen et al reported that FBXL2 is ectopically expressed in a transformed murine lung epithelial (MLE) cell line. Ectopic expression of FBXL2 induces cyclin D2 degradation, whereas knockdown of FBXL2 results in signicant increase in cyclin D2 expression.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA SMARCA5 inhibits gastric cancer progression through targeting the miR-346/ FBXL2 axis

Tang

et al. 2019

RSC Adv.

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“…Cdh1 stimulated degradation of FoxM1 protein in HeLa 49 , U2OS 17 , and MCF-7 cells 50 . Moreover, Fbxl2 (a component of Skp-Cullin-F box ubiquitin E3 ligase) 51 and VprBP (a component of cullin 4-based E3 ubiquitin ligase) 52 have been reported to regulate the degradation of FoxM1 in different cells. Here we discovered that FoxM1 directly interacted with Cdh1, rather than the adaptor Cdc20.…”

Section: Discussionmentioning

confidence: 99%

A Cdh1–FoxM1–Apc axis controls muscle development and regeneration

Chen

et al. 2020

Cell Death Dis

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Forkhead box M1 (FoxM1) transcriptional factor has a principal role in regulating cell proliferation, self-renewal, and tumorigenesis. However, whether FoxM1 regulates endogenous muscle development and regeneration remains unclear. Here we found that loss of FoxM1 in muscle satellite cells (SCs) resulted in muscle atrophy and defective muscle regeneration. FoxM1 functioned as a direct transcription activator of adenomatous polyposis coli (Apc), preventing hyperactivation of wnt/β-catenin signaling during muscle regeneration. FoxM1 overexpression in SCs promoted myogenesis but impaired muscle regeneration as a result of spontaneous activation and exhaustion of SCs by transcriptional regulation of Cyclin B1 (Ccnb1). The E3 ubiquitin ligase Cdh1 (also termed Fzr1) was required for FoxM1 ubiquitylation and subsequent degradation. Loss of Cdh1 promoted quiescent SCs to enter into the cell cycle and the SC pool was depleted by serial muscle injuries. Haploinsufficiency of FoxM1 ameliorated muscle regeneration of Cdh1 knock-out mice. These data demonstrate that the Cdh1-FoxM1-Apc axis functions as a key regulator of muscle development and regeneration.

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F‐box protein FBXL2 inhibits gastric cancer proliferation by ubiquitin‐mediated degradation of forkhead box M1

Cited by 28 publications

References 25 publications

miRNA-346 promotes proliferation, migration and invasion in liver cancer

miRNA-346 promotes proliferation, migration and invasion in liver cancer

Circular RNA SMARCA5 inhibits gastric cancer progression through targeting the miR-346/ FBXL2 axis

A Cdh1–FoxM1–Apc axis controls muscle development and regeneration

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