Overexpression of NuSAP1 is predictive of an unfavourable prognosis and promotes proliferation and invasion of triple-negative breast cancer cells via the Wnt/β-catenin/EMT signalling axis

Sun, Li; Shi, Changlong; Liu, Shaozhuang; Zhang, Enchong; Long, Yan; Ji, Ce; Zhao, Yi

doi:10.1016/j.gene.2020.144657

Cited by 28 publications

(22 citation statements)

References 38 publications

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“…Due to the lack of effective targeted therapy drugs, TNBC was an aggressive malignant tumor [ 15 ]. Also, the survival rates of TNBC patients are still the shortest among all breast cancer subtypes [ 16 ]. TNBC is prone to bone metastasis, and the liposome-mediated targeted therapy has a good effect [ 17 , 18 ].…”

Section: Discussionmentioning

confidence: 99%

Cyclin B2 (CCNB2) Stimulates the Proliferation of Triple-Negative Breast Cancer (TNBC) Cells In Vitro and In Vivo

Jia

2021

Disease Markers

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Triple-negative breast cancer (TNBC) is the most aggressive type of breast cancer. Currently, targeting therapy makes great advances for the treatment of TNBC, whereas more effective therapeutic targets are urgently needed. Cyclin B2 (CCNB2), which belongs to B-type cyclins, is known as a cell cycle regulator. CCNB2 is synthesized at G1 phase in cancer cells and downregulated at anaphase. The defects of CCNB2 led to the abnormal cell cycle and tumorigenesis. Though there are wide effects of CCNB2 on multiple types of tumors, the potential role of CCNB2 in TNBC progression is still unclear. Herein, we found that CCNB2 was highly expressed in human TNBC tissues and correlated with the prognosis and clinical pathological features including tumor size ( p = 0.022 ∗ ) and pTNM stage ( p = 0.021 ∗ ) of patients with TNBC. CCNB2 could promote the proliferation of TNBC cells in vitro and in mice. Our findings therefore confirmed the involvement of CCNB2 in TNBC progression and provided the evidence that CCNB2 could serve as a promising molecular target of TNBC.

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Section: Discussionmentioning

confidence: 99%

Cyclin B2 (CCNB2) Stimulates the Proliferation of Triple-Negative Breast Cancer (TNBC) Cells In Vitro and In Vivo

Jia

2021

Disease Markers

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“…NuSAP1 is a microtubule-binding protein involved in several types of cancers such as prostate cancer, colorectal cancer, and astrocytoma [ 28 - 30 ]. Previous studies found that high expression of NuSAP1 was significantly correlated with poor prognosis of breast cancer and melanoma [ 17 ]. NuSAP1 was also previously reported to be highly expressed in breast cancer and involved in breast cancer progression [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have found that NuSAP1 was overexpressed in several types of cancers such as prostate cancer, colorectal cancer, and astrocytoma [14][15][16]. NuSAP1 also served as a key regulator of breast cancer progression, and it contributed to cell proliferation and invasion [17]. High expression of NuSAP1 was correlated with poor prognosis of breast cancer and melanoma [18].…”

Section: Introductionmentioning

confidence: 99%

ANKRD22 enhances breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression

Liu

Gong

et al. 2020

Bosn J of Basic Med Sci

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Breast cancer is one of the most prevalent malignancies in women worldwide. Although great progress has been achieved in the diagnosis and treatment of breast cancer, the prognosis of patients with breast cancer is still poor due to distal recurrence and metastasis after surgery. This study demonstrated that the expression level of ankyrin repeat domain 22 (ANKRD22) in human breast cancer tissues was significantly higher than that in normal breast tissues. ANKRD22 knockdown inhibited the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells. Further research indicated that ANKRD22 regulated the expression of nucleolar and spindle-associated protein 1 (NuSAP1) and then the activation of Wnt/β-catenin signaling pathway. Moreover, overexpression of NuSAP1 reversed the inhibitory effects of ANKRD22 knockdown on the proliferation, invasion, and EMT of breast cancer cells. In summary, this study demonstrated that ANKRD22 enhanced breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression, which might shed light on new therapeutic approaches for breast cancer.

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“…Interestingly, amongst the most significant C28modulated hits was NUSAP1 (P < 0.05 and Log2 fold change of ≥|1.25|), a microtubule associated protein participating in mitotic spindle organization [8,9], whose role has been closely associated with tumour progression, chemoresistance, and poor prognosis in many tumours including BC [10,11]. The effects of C28 on NUSAP1 were validated in additional BC cell lines (Fig.…”

Section: Pharmacological or Genetic Inhibition Of Lmtk3 Downregulatesmentioning

confidence: 96%

LMTK3 inhibition affects microtubule stability

et al. 2021

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Overexpression of NuSAP1 is predictive of an unfavourable prognosis and promotes proliferation and invasion of triple-negative breast cancer cells via the Wnt/β-catenin/EMT signalling axis

Cited by 28 publications

References 38 publications

Cyclin B2 (CCNB2) Stimulates the Proliferation of Triple-Negative Breast Cancer (TNBC) Cells In Vitro and In Vivo

Cyclin B2 (CCNB2) Stimulates the Proliferation of Triple-Negative Breast Cancer (TNBC) Cells In Vitro and In Vivo

ANKRD22 enhances breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression

LMTK3 inhibition affects microtubule stability

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