LINC01857 as an oncogene regulates CREB1 activation by interacting with CREBBP in breast cancer

Xiong, Youyi; Gu, Yuanting; Wang, Fang; Li, Lin; Zhu, Mingzhi; Wang, Nan; Mi, Hailong; Qiu, Xinguang

doi:10.1002/jcp.28090

Cited by 26 publications

(20 citation statements)

References 26 publications

(40 reference statements)

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“… 25 Additionally, a recent study also showed that LINC01857 transcriptionally activates CREB1 expression through associating with CREBBP protein in BC and promotes tumor progression. 26 LCPAT1 has been reported to promote lung cancer cell proliferation, and it participates in DNA damage. 17 , 27 To our knowledge, whether LCPAT1 is involved in BC regulation remains totally unclear.…”

Section: Discussionmentioning

confidence: 99%

lncRNA LCPAT1 Upregulation Promotes Breast Cancer Progression via Enhancing MFAP2 Transcription

Gong

Dong

Niu

et al. 2020

Molecular Therapy - Nucleic Acids

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The importance of long noncoding RNA (lncRNA) in tumorigenesis has been supported by increasing evidence in recent years. However, the mechanism linking lncRNA function with cancer progression remains poorly understood. lncRNA LCPAT1 plays a role in lung cancer. However, how it works in breast cancer (BC) is largely unclear. In this study, we found that LCPAT1 was highly expressed in BC tissues and cell lines. High LCPAT1 expression predicted a low survival rate in BC patients. LCPAT1 promoted BC cell proliferation, migration, and invasion while inhibiting apoptosis in vitro . LCPAT1 knockdown suppressed BC growth in vivo and vice versa. LCPAT1 interacted with RBBP4 and recruited it to the MFAP2 (microfibril-associated protein 2) promoter and then activated MFAP2 transcription. Restoration of MFAP2 rescued the effects of LCPAT1 knockdown in BC cells. In sum, LCPAT1 promotes BC progression through recruiting RBBP4 to initiate MFAP2 transcription.

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Section: Discussionmentioning

confidence: 99%

lncRNA LCPAT1 Upregulation Promotes Breast Cancer Progression via Enhancing MFAP2 Transcription

Gong

Dong

Niu

et al. 2020

Molecular Therapy - Nucleic Acids

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“…16 In addition, increased expression of LINC01857, a CREB1 activator, was found to be linked to reduced survival time in patients with breast cancer. 17 As for in GC, an inhibitor of CREB1, miR-1297, was found to be poorly existed in GC patients and positively correlated with survival of patients. 18 Promotion of CREB1 in cancer has also been evidenced in several tumor cell types involving bladder cancer, 19 colorectal cancer 20 and glioma 21 cells.…”

Section: Discussionmentioning

confidence: 93%

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Huang

Liu

Jiang

et al. 2020

CMAR

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Background: The cAMP response element-binding protein 1 (CREB1) was initiated as a potential target for cancer treatment. This research was conducted to probe the effect of CREB1 in the progression of gastric cancer (GC) and the molecules involved. Materials and Methods: CREB1 expression in GC tissues and cell lines (AGS and MKN-45) as well as that in normal tissues and in gastric mucosa cell line (GES-1) was detected. The correlation between CREB1 expression and prognosis of GC patients was determined. Artificial silencing of CREB1 was introduced to evaluate its effect on biological behaviors of GC cells. The target microRNA (miRNA) of CREB1 and the target mRNA of miR-186 were predicted and validated. Altered expression of miR-186, KRT8 and HIF-1α was introduced to confirm their functions in GC progression. Results: CREB1 was abundantly expressed in GC tissues and cells and linked to dismal prognosis in patients. Silencing of CREB1 or upregulation of miR-186 suppressed the malignant behaviors such as growth, epithelial-mesenchymal transition (EMT) and invasion of GC cells, while artificial overexpression of KRT8 led to reversed trends. KRT8 was a target mRNA of miR-186, and CREB1 transcriptionally suppressed miR-186 expression to further up-regulate KRT8. KRT8 was also found to increase HIF-1α expression. Upregulation of HIF-1α was found to block the suppressing role of CREB1 silencing in GC cell malignancy. Conclusion: This study evidenced that silencing of CREB1 inhibits growth, invasion, EMT and resistance to apoptosis of GC cells involving the upregulation of miR-186 and the following downregulation of KRT8 and HIF-1α.

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“…We also found that LINC01857, LINC02446, and LINC02384, as protective factors of IL2R and IL7R, were potential oncogenic molecules, while miR‐203b‐3p and miR‐891a‐5p were suppressive of IL2RA and IL7R respectively. At present, there are still no reports about LINC01857 in malignant melanoma, and three reports indicating that LINC01857 was a potential oncogene in glioma, 40 breast cancer 41 and pancreatic cancer. 42 At the same time, there are no related literature on LINC02446 and LINC02384.…”

Section: Discussionmentioning

confidence: 99%

Pivotal factors associated with the immunosuppressive tumor microenvironment and melanoma metastasis

et al. 2021

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LINC01857 as an oncogene regulates CREB1 activation by interacting with CREBBP in breast cancer

Cited by 26 publications

References 26 publications

lncRNA LCPAT1 Upregulation Promotes Breast Cancer Progression via Enhancing MFAP2 Transcription

lncRNA LCPAT1 Upregulation Promotes Breast Cancer Progression via Enhancing MFAP2 Transcription

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Pivotal factors associated with the immunosuppressive tumor microenvironment and melanoma metastasis

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