Friend leukemia virus integration 1 is a predictor of poor prognosis of breast cancer and promotes metastasis and cancer stem cell properties of breast cancer cells

Xu, Yan; Yu, Yu; Li, Lingyu; Chen, Naifei; Song, Wei; He, Hua; Dong, Jie; Liu, Xiangliang; Cui, Jiuwei

doi:10.1002/cam4.1589

Cited by 20 publications

(15 citation statements)

References 40 publications

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“…FLI1 was first identified as an ETS family member protein that plays a vital role in retroviral-mediated acute leukemias. 45 Accumulating evidence suggested that FLI1 also accelerated the metastasis of nasopharyngeal carcinoma (NPC), 46 breast cancer, 47 and small cell lung cancer, 48 among others. Meanwhile, FLI1 has been well documented to act as an oncogene in Ewing sarcoma.…”

Section: Discussionmentioning

confidence: 99%

circCAMSAP1 promotes osteosarcoma progression and metastasis by sponging miR-145-5p and regulating FLI1 expression

Chen

Zhang

et al. 2021

Molecular Therapy - Nucleic Acids

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Osteosarcoma is the most common primary malignant bone tumor in adolescents. While chemotherapy combined with surgery can improve the prognosis of some patients, chemo-resistance is still a huge obstacle in osteosarcoma treatment. Accumulating evidence demonstrates that circular RNAs (circRNAs) are involved in cancer progression and metastasis, but their specific role in osteosarcoma remains mostly undescribed. In this study, we performed circRNA deep sequencing and identified 88 distinct circRNAs from a human osteosarcoma cell lines group (143B, HOS, SJSA, and U2OS) and the human osteoblast hFOB 1.19 (control). We found that circCAMSAP1, also named hsa_circ_0004338, is significantly upregulated in human osteosarcoma tissues and cell lines, and it is positively correlated with osteosarcoma development. Silencing of circCAMSAP1 effectively suppresses osteosarcoma cell growth, apoptosis, migration, and invasion. Furthermore, we validated that circCAMSAP1 functions in osteosarcoma tumorigenesis through a circCAMSAP1/miR-145-5p/friend leukemia virus integration 1 (FLI1) pathway. FLI1 promotes osteosarcoma tumorigenesis and miR-145-5p suppresses FLI translation. circCAMSAP1 directly sequesters miR-145-5p in the cytoplasm and inhibits its activity to suppress osteosarcoma tumorigenesis. Moreover, the regulatory role of circCAMSAP1 upregulation was examined and validated in rats. In summary, our findings provide evidence that circCAMSAP1 act as a “microRNA sponge” and suggest a new therapeutic target of human osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

circCAMSAP1 promotes osteosarcoma progression and metastasis by sponging miR-145-5p and regulating FLI1 expression

Chen

Zhang

et al. 2021

Molecular Therapy - Nucleic Acids

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“…In PE, when CS are elevated, Na/K-ATPase is depressed and Fli1 is low this results in the occurrence of a phenotype associated with a significantly lower incidence of breast cancer [ 59 , 60 ] ( Figure 2 ). At the same time in breast cancer patients ( Figure 2 ) CS and Na/K-ATPase are regular [ 61 , 62 , 63 , 64 , 65 ] and Fli1 is high [ 66 , 67 , 68 ]; i.e., as if patients with PE administered an anti-CS antibody. Could it be true for the other types of cancer?…”

Section: Immunoneutralization Of Cardiotonic Steroidsmentioning

confidence: 99%

“…When levels of MBG are increased, levels of Fli1 decrease and a Col-1 gene promoter is released from the nucleus and procollagen-1 and collagen become activated [ 32 ]. While many studies have demonstrated that Fli1 is a pro-cancer factor [ 68 , 69 ], CS including MBG are becoming attractive anti-cancer drug candidates [ 70 , 71 ]. It is generally accepted that PE is associated with a low risk of cancer, which is not surprising considering that endogenous levels of MBG and other CS are dramatically increased in PE patients [ 27 , 28 ] and therefore suppress the growth of tumors in vivo and in vitro [ 72 , 73 , 74 ].…”

Section: Interaction Of Cs and Fli1 And A Hint For Cancermentioning

confidence: 99%

Preeclampsia: Cardiotonic Steroids, Fibrosis, Fli1 and Hint to Carcinogenesis

Agalakova

Kolodkin

Adair

et al. 2021

IJMS

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Despite prophylaxis and attempts to select a therapy, the frequency of preeclampsia does not decrease and it still takes the leading position in the structure of maternal mortality and morbidity worldwide. In this review, we present a new theory of the etiology and pathogenesis of preeclampsia that is based on the interaction of Na/K-ATPase and its endogenous ligands including marinobufagenin. The signaling pathway of marinobufagenin involves an inhibition of transcriptional factor Fli1, a negative regulator of collagen synthesis, followed by the deposition of collagen in the vascular tissues and altered vascular functions. Moreover, in vitro and in vivo neutralization of marinobufagenin is associated with the restoration of Fli1. The inverse relationship between marinobufagenin and Fli1 opens new possibilities in the treatment of cancer; as Fli1 is a proto-oncogene, a hypothesis on the suppression of Fli1 by cardiotonic steroids as a potential anti-tumor therapeutic strategy is discussed as well. We propose a novel therapy of preeclampsia that is based on immunoneutralization of the marinobufagenin by monoclonal antibodies, which is capable of impairing marinobufagenin-Na/K-ATPase interactions.

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“…Interestingly, when levels of CS were compared in the nude mice expressed significantly lower CS concentrations in the adrenal gland and the plasma compared to normal mice [67]. The nude mouse is valuable to research because it can receive many different types of tissue and tumor grafts, as it mounts no rejection response, and it has a very high prognostic value of FLI1 [68,69].…”

Section: Interaction Of Cs and Fli1 And A Hint For Cancermentioning

confidence: 99%

Preeclampsia: Сardiotonic Steroids, Fibrosis and a Hint to Cancerogenesis

Багров¹,

Kolodkin²,

Adair³

et al. 2020

Preprint

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Despite prophylaxis and attempts to select a therapy, the frequency of preeclampsia does not decrease, and it still takes the leading position in the structure of maternal mortality and morbidity worldwide. In this review, we present a new theory of the etiology and pathogenesis of preeclampsia which is based on the interaction of Na/K-ATPase and its endogenous ligands including marinobufagenin. The signaling pathway of marinobufagenin involves an inhibition of transcriptional factor Fli1, a negative regulator of collagen synthesis, followed by deposition of collagen in the vascular tissues and altered vascular functions. Moreover, in vitro and in vivo neutralization of marinobufagenin is associated with restoration of Fli1. The inverse relationship between marinobufagenin and Fli1 opens new possibilities in the treatment of cancer: since Fli1 is a proto-oncogene, a hypothesis on suppression of Fli1 by cardiotonic steroids as potential anti-tumor therapeutic strategy is discussed as well. We propose a novel therapy of preeclampsia which is based on immunoneutralization of the marinobufagenin by monoclonal antibodies, which is capable to impair marinobufagenin-Na/K-ATPase interactions.

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Friend leukemia virus integration 1 is a predictor of poor prognosis of breast cancer and promotes metastasis and cancer stem cell properties of breast cancer cells

Cited by 20 publications

References 40 publications

circCAMSAP1 promotes osteosarcoma progression and metastasis by sponging miR-145-5p and regulating FLI1 expression

circCAMSAP1 promotes osteosarcoma progression and metastasis by sponging miR-145-5p and regulating FLI1 expression

Preeclampsia: Cardiotonic Steroids, Fibrosis, Fli1 and Hint to Carcinogenesis

Preeclampsia: Сardiotonic Steroids, Fibrosis and a Hint to Cancerogenesis

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