FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis

Yang, Hua; Ren, Lili; Wang, Yanan; Bi, Xuebing; Li, Xiaoli; Wen, Min; Zhang, Qian; Yang, Yang; Jia, Yongsheng; Li, Yumiao; Zang, Aimin; Wei, Yuying; Dai, Guanghai

doi:10.1038/s41419-020-03053-0

Cited by 39 publications

(36 citation statements)

References 54 publications

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“…( 59 ), Yang et al. ( 60 ), and Li et al. ( 61 ) showed that miR-140-3p, miR-30c, and miR-148a can inhibit the expression of PXR and CYP3A4, respectively, by acting on the 3’UTR of PXR and reduce the elimination of anti-cancer agents in tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Hsa-miR-4277 Decelerates the Metabolism or Clearance of Sorafenib in HCC Cells and Enhances the Sensitivity of HCC Cells to Sorafenib by Targeting cyp3a4

Sun

Jiang

et al. 2021

Front. Oncol.

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Increasing evidence has shown that the metabolism and clearance of molecular targeted agents, such as sorafenib, plays an important role in mediating the resistance of HCC cells to these agents. Metabolism of sorafenib is performed by oxidative metabolism, which is initially mediated by CYP3A4. Thus, targeting CYP3A4 is a promising approach to enhance the sensitivity of HCC cells to chemotherapeutic agents. In the present work, we examined the association between CYP3A4 and the prognosis of HCC patients receiving sorafenib. Using the online tool miRDB, we predicted that has-microRNA-4277 (miR-4277), an online miRNA targets the 3’UTR of the transcript of cyp3a4. Furthermore, overexpression of miR-4277 in HCC cells repressed the expression of CYP3A4 and reduced the elimination of sorafenib in HCC cells. Moreover, miR-4277 enhanced the sensitivity of HCC cells to sorafenib in vitro and in vivo. Therefore, our results not only expand our understanding of CYP3A4 regulation in HCC, but also provide evidence for the use of miR-4277 as a potential therapeutic in advanced HCC.

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Section: Discussionmentioning

confidence: 99%

Hsa-miR-4277 Decelerates the Metabolism or Clearance of Sorafenib in HCC Cells and Enhances the Sensitivity of HCC Cells to Sorafenib by Targeting cyp3a4

Sun

Jiang

et al. 2021

Front. Oncol.

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“…The use of clinical specimens was approved by the ethics committee of the Beijing Tian Tan Hospital, Capital Medical University. The 30 clinical TNBC specimens (the BRCA mutation subtype) and paired non-tumor tissues were described in our previous publication ( 35 ). The usage of the clinical specimens were with the written consent from patients and all the experiments related to the human-derived materials, including clinical specimens and cell lines, were used in accordance with the Helsinki Declaration with the approval from medical ethic committee of Beijing Tiantan Hospital or the/the Hebei Key Laboratory of the Cancer Radiotherapy and Chemotherapy.…”

Section: Methodsmentioning

confidence: 99%

“…: S1060), was purchased from Selleck Corporation, Houston, Texas, US. The formulations of olaparib used in the cell-based experiments or animal experiments were described in our previous publication ( 35 ).…”

Section: Methodsmentioning

confidence: 99%

“…It can recognize and bind to the 3’UTR of the target mRNA and degrade the mRNA to achieve gene silencing ( 33 , 34 ). The use of miRNA to inhibit the expression of tumor-related genes has emerged as an important strategy for antitumor therapy ( 35 ). The γ-Secretase is a complex containing multiple protein subunits, including PSEN-1, the catalytic center; Pen-2, the activity regulator subunit; and NCSTN, to stabilize the complex ( 21 ).…”

Section: Introductionmentioning

confidence: 99%

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miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase

et al. 2021

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Olaparib has been used in the treatment of triple-negative breast cancer (TNBC) with BRCA mutations. In the present study, we demonstrated the effect of miR-27-3p on the γ-secretase pathway by regulating the sensitivity of TNBC cells to olaparib. miR-27-3p, a microRNA with the potential to target PSEN-1, the catalytic subunit of γ-secretase mediating the second step of the cleavage of the Notch protein, was identified by the online tool miRDB and found to inhibit the expression of PSEN-1 by directly targeting the 3’-untranslated region (3’-UTR) of PSEN-1. The overexpression of miR-27-3p inhibited the activation of the Notch pathway via the inhibition of the cleavage of the Notch protein, mediated by γ-secretase, and, in turn, enhanced the sensitivity of TNBC cells to the antitumor agent olaparib. Transfection with PSEN-1 containing mutated targeting sites for miR-27-3p or the expression vector of the Notch protein intracellular domain (NICD) almost completely blocked the effect of miR-27-3p on the Notch pathway or the sensitivity of TNBC cells to olaparib, respectively. Therefore, our results suggest that the miR-27-3p/γ-secretase axis participates in the regulation of TNBC and that the overexpression of miR-27-3p represents a potential approach to enhancing the sensitivity of TNBC to olaparib.

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“…Hepatocellular carcinoma (HCC) accounts for the vast majority of liver cancers, representing nearly 75% of all primary liver tumors ( 4 – 6 ). The geographic regions with the highest incidence of HCC are Asia and Africa, and nearly half of all cases are estimated to occur in China ( 7 – 10 ). The most effective treatment for liver cancer is presently surgical resection.…”

Section: Introductionmentioning

confidence: 99%

CK-3, A Novel Methsulfonyl Pyridine Derivative, Suppresses Hepatocellular Carcinoma Proliferation and Invasion by Blocking the PI3K/AKT/mTOR and MAPK/ERK Pathways

Liu

et al. 2021

Front. Oncol.

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Hepatocellular carcinoma (HCC) is an aggressive tumor with a poor prognosis that highly expresses phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (ERK). The PI3K/AKT/mTOR and MAPK/ERK signaling pathways play a crucial role in HCC tumor formation, cell cycle, apoptosis and survival. However, no effective targeted therapies against these pathways is available, mainly due to the extensive and complex negative feedback loops between them. Here we used CK-3, a dual blocker of the PI3K/AKT/mTOR and MAPK/ERK pathways, against HCC cell lines to verify its anti-tumor activity in vitro. CK-3 exhibited cytotoxic activity against HCC, as demonstrated with MTT and colony formation assays. The anti-metastatic potential of CK-3 was demonstrated with wound healing and cell invasion assays. The ability of CK-3 to block both the PI3K/AKT/mTOR and MAPK/ERK pathways was also confirmed. CK-3 induced the apoptosis of Hep3B cells, while Bel7402 cells died via mitotic catastrophe (MC). Oral administration of CK-3 also inhibited the subcutaneous growth of BEL7402 cells in nude mice. Simultaneous PI3K/AKT/mTOR and MAPK/ERK pathway inhibition with CK-3 may be superior to single pathway monotherapies by inhibiting their feedback-regulation, and represents a potential treatment for HCC.

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FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis

Cited by 39 publications

References 54 publications

Hsa-miR-4277 Decelerates the Metabolism or Clearance of Sorafenib in HCC Cells and Enhances the Sensitivity of HCC Cells to Sorafenib by Targeting cyp3a4

Hsa-miR-4277 Decelerates the Metabolism or Clearance of Sorafenib in HCC Cells and Enhances the Sensitivity of HCC Cells to Sorafenib by Targeting cyp3a4

miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase

CK-3, A Novel Methsulfonyl Pyridine Derivative, Suppresses Hepatocellular Carcinoma Proliferation and Invasion by Blocking the PI3K/AKT/mTOR and MAPK/ERK Pathways

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