LINC00160 mediated paclitaxel‐And doxorubicin‐resistance in breast cancer cells by regulating TFF3 <i>via</i> transcription factor C/EBPβ

Wu, Huaiguo; Gu, Juan; Zhou, Dachen; Cheng, Wei; Wang, Yueping; Wang, Qingping; Wang, Xuedong

doi:10.1111/jcmm.15487

Cited by 38 publications

(20 citation statements)

References 42 publications

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“… 14 Increasingly evidence in recent years have indicated that lncRNAs are associated with tumor progression and drug resistance. 6 , 9 , 10 Hence, studying lncRNA is useful to understand the mechanisms relevant to BC progression. This work focused on the regulatory mechanism of LINC00665 in BC with the aim to provide novel insights into the pathogenesis of BC.…”

Section: Discussionmentioning

confidence: 99%

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LINC00665 Stimulates Breast Cancer Progression via Regulating miR-551b-5p

Sun²,

Yang³

et al. 2021

CMAR

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Introduction Long intergenic non-protein coding RNA 665 (LINC00665) has been revealed to contribute cancer progression in many cancer types including liver and gastric cancer. However, the roles of LINC00665 in breast cancer (BC) remain to be explored. Methods We explored LINC00665 expression in BC tissues and normal tissues at GEPIA. Then, its expression in BC cells (HCC-1937, MDA-MB-231, and MCF-7) and normal cells (MCF10A) was analyzed with qRT-PCR. In addition, the mechanisms of LINC00665 in BC were explored using bioinformatic analyses, luciferase activity reporter assay, RNA pull-down assay, and rescue experiments. Results We showed LINC00665 expression was significantly increased in both BC tissues and cells. The knockdown of LINC00625 significantly inhibits BC cell growth and promotes cell apoptosis in vitro, while the overexpression of LINC00625 has the opposite effects on BC progression. LINC00665 could affect BC progression via regulating miR-551b-5p. Discussion Taken together, our study showed that the LINC00665/miR-551b-5p axis was involved in the progression of BC.

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Section: Discussionmentioning

confidence: 99%

“… 6 LINC00160 may affect the response of BC cells to chemical reagents including paclitaxel and doxorubicin by regulating TFF3 expression. 9 LncRNA DLX6-AS1 could regulate the epithelial-mesenchymal transition process of BC cells and their sensitivity to cisplatin via regulating miR-199b-5p. 10 …”

Section: Introductionmentioning

confidence: 99%

LINC00665 Stimulates Breast Cancer Progression via Regulating miR-551b-5p

Sun²,

Yang³

et al. 2021

CMAR

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“…Past studies [10,19,27] have implicated ATF5, CEBPB and CEBPD in the regulation of cancer cell responsiveness to the microtubule-targeting drug Taxol (paclitaxel), which is used to treat breast and other tumor types. We therefore compared responses of MCF7 and triple negative MDA-MB-231 breast cancer cells to Taxol either alone or in combination with Dpep and Bpep.…”

Section: Bpep and Dpep Act In Combination With Other Cancer Therapeuticsmentioning

confidence: 99%

Cell-Penetrating CEBPB and CEBPD Leucine Zipper Decoys as Broadly Acting Anti-Cancer Agents

Zhou

Sun

Pasquier

et al. 2021

Cancers

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Transcription factors are key players underlying cancer formation, growth, survival, metastasis and treatment resistance, yet few drugs exist to directly target them. Here, we characterized the in vitro and in vivo anti-cancer efficacy of novel synthetic cell-penetrating peptides (Bpep and Dpep) designed to interfere with the formation of active leucine-zipper-based dimers by CEBPB and CEBPD, transcription factors implicated in multiple malignancies. Both peptides similarly promoted apoptosis of multiple tumor lines of varying origins, without such effects on non-transformed cells. Combined with other treatments (radiation, Taxol, chloroquine, doxorubicin), the peptides acted additively to synergistically and were fully active on Taxol-resistant cells. The peptides suppressed expression of known direct CEBPB/CEBPD targets IL6, IL8 and asparagine synthetase (ASNS), supporting their inhibition of transcriptional activation. Mechanisms by which the peptides trigger apoptosis included depletion of pro-survival survivin and a required elevation of pro-apoptotic BMF. Bpep and Dpep significantly slowed tumor growth in mouse models without evident side effects. Dpep significantly prolonged survival in xenograft models. These findings indicate the efficacy and potential of Bpep and Dpep as novel agents to treat a variety of cancers as mono- or combination therapies.

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“…Then, an increase occurs in glycolysis, providing condition for DOX resistance [16]. Non-coding RNAs (ncRNAs) such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) also participate in development of DOX resistance due to their regulatory effects on biological mechanisms and molecular pathways [17][18][19][20][21]. In addition to recognition of tumor-promoting molecular pathways and using combination chemotherapy, another strategy that utilizes nanostructures for DOX delivery has been developed.…”

Section: Introductionmentioning

confidence: 99%

Nrf2 Signaling Pathway in Chemoprotection and Doxorubicin Resistance: Potential Application in Drug Discovery

et al. 2021

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Doxorubicin (DOX) is extensively applied in cancer therapy due to its efficacy in suppressing cancer progression and inducing apoptosis. After its discovery, this chemotherapeutic agent has been frequently used for cancer therapy, leading to chemoresistance. Due to dose-dependent toxicity, high concentrations of DOX cannot be administered to cancer patients. Therefore, experiments have been directed towards revealing underlying mechanisms responsible for DOX resistance and ameliorating its adverse effects. Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling is activated to increase levels of reactive oxygen species (ROS) in cells to protect them against oxidative stress. It has been reported that Nrf2 activation is associated with drug resistance. In cells exposed to DOX, stimulation of Nrf2 signaling protects cells against cell death. Various upstream mediators regulate Nrf2 in DOX resistance. Strategies, both pharmacological and genetic interventions, have been applied for reversing DOX resistance. However, Nrf2 induction is of importance for alleviating side effects of DOX. Pharmacological agents with naturally occurring compounds as the most common have been used for inducing Nrf2 signaling in DOX amelioration. Furthermore, signaling networks in which Nrf2 is a key player for protection against DOX adverse effects have been revealed and are discussed in the current review.

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LINC00160 mediated paclitaxel‐And doxorubicin‐resistance in breast cancer cells by regulating TFF3 via transcription factor C/EBPβ

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 38 publications

References 42 publications

LINC00665 Stimulates Breast Cancer Progression via Regulating miR-551b-5p

LINC00665 Stimulates Breast Cancer Progression via Regulating miR-551b-5p

Cell-Penetrating CEBPB and CEBPD Leucine Zipper Decoys as Broadly Acting Anti-Cancer Agents

Nrf2 Signaling Pathway in Chemoprotection and Doxorubicin Resistance: Potential Application in Drug Discovery

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