FOXM1 evokes 5-fluorouracil resistance in colorectal cancer depending on ABCC10

Xie, Tao; Geng, Jiao; Wang, Ye; Wang, Liya; Huang, Mengxi; Chen, Jing; Zhang, Kai; Xue, Lijun; Liu, Fei; Mao, Xiaobei; Chen, Yanan; Wang, Qin; Dai, Tingting; Ren, Lili; Yu, Hong-Ju; Wang, Rui; Chen, Longbang; Chen, Cheng; Chen, Xiaoyuan

doi:10.18632/oncotarget.14351

Cited by 65 publications

(57 citation statements)

References 43 publications

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“…Through TEAD interaction YAP controls a set of genes such as CTGF, cyr61, survivin, amphiregulin and AXL [11,14,46], and some of them have been associated with drug resistance [47]. [12], and it has been related to the drug resistance in a variety of cancers [48][49][50].…”

Section: Discussionmentioning

confidence: 99%

Crosstalk between Nrf2 and YAP contributes to maintaining the antioxidant potential and chemoresistance in bladder cancer

Ciamporcero

Daga

Pizzimenti

et al. 2018

Free Radical Biology and Medicine

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Redox adaptation plays an important role in cancer cells drug resistance. The antioxidant response is principally mediated by the transcription factor Nrf2, that induces the transcriptional activation of several genes involved in GSH synthesis, chemoresistance, and cytoprotection. YAP is emerging as a key mediator of chemoresistance in a variety of cancers, but its role in controlling the antioxidant status of the cells is yet elusive. Here, we show that impairing YAP protein expression reduced GSH content and Nrf2 protein and mRNA expression in bladder cancer cells. Moreover, in YAP knocked down cells the expression of FOXM1, a transcription factor involved in Nrf2 transcription, was down-regulated and the silencing of FOXM1 reduced Nrf2 expression. On the other hand, the silencing of Nrf2, as well as the depletion of GSH by BSO treatment, inhibited YAP expression, suggesting that cross-talk exists between YAP and Nrf2 proteins. Importantly, we found that silencing either YAP or Nrf2 enhanced sensitivity of bladder cancer cells to cytotoxic agents and reduced their migration. Furthermore, the inhibition of both YAP and Nrf2 expressions significantly increased cytotoxic drug sensitivity and synergistically reduced the migration of chemoresistant bladder cancer cells. These findings provide a rationale for targeting these transcriptional regulators in patients with chemoresistant bladder cancer, expressing high YAP and bearing a proficient antioxidant system.

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Section: Discussionmentioning

confidence: 99%

Crosstalk between Nrf2 and YAP contributes to maintaining the antioxidant potential and chemoresistance in bladder cancer

Ciamporcero

Daga

Pizzimenti

et al. 2018

Free Radical Biology and Medicine

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“…Consistent with these data, inhibition of FOXM1 and/or ABCC10 sensitizes resistant CRC cells to 5‐FU. Thus, the FOXM1/ABCC10 axis might be a new potential therapeutic target to counteract 5‐FU resistance in CRC 44 …”

Section: Multidrug Resistance and Membrane Drug Transportersmentioning

confidence: 99%

5‐Fluorouracil resistance mechanisms in colorectal cancer: From classical pathways to promising processes

et al. 2020

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Colorectal cancer (CRC) is a public health problem. It is the third most common cancer in the world, with nearly 1.8 million new cases diagnosed in 2018. The only curative treatment is surgery, especially for early tumor stages. When there is locoregional or distant invasion, chemotherapy can be introduced, in particular 5‐fluorouracil (5‐FU). However, the disease can become tolerant to these pharmaceutical treatments: resistance emerges, leading to early tumor recurrence. Different mechanisms can explain this 5‐FU resistance. Some are disease‐specific, whereas others, such as drug efflux, are evolutionarily conserved. These mechanisms are numerous and complex and can occur simultaneously in cells exposed to 5‐FU. In this review, we construct a global outline of different mechanisms from disruption of 5‐FU‐metabolic enzymes and classic cellular processes (apoptosis, autophagy, glucose metabolism, oxidative stress, respiration, and cell cycle perturbation) to drug transporters and epithelial‐mesenchymal transition induction. Particular interest is directed to tumor microenvironment function as well as epigenetic alterations and miRNA dysregulation, which are the more promising processes that will be the subject of much research in the future.

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“…ABCC10 is a member of the ATP-binding cassette (ABC) transporter superfamily, which is also named multidrug resistance associated protein 7 (MRP7). ABCC10 is well characterized with drug resistance; it acts as an efflux pump to transport anticancer drugs out of the cells before they reach the cytosol [26,27]. Accordingly, we speculated that FENDRR depressed DDP resistance by inhibiting ABCC10 expression in A549/DDP.…”

Section: Discussionmentioning

confidence: 94%

Long non-coding RNA FOXF1 adjacent non-coding developmental regulatory RNA inhibits growth and chemotherapy resistance in non-small cell lung cancer

Xu¹

2019

aoms

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Introduction: Lung cancer is one of the most common malignant neoplasms around the globe. Its most common type is non-small cell lung cancer (NSCLC). The FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR) gene is an lncRNA which has been reported to show low expression and a tumor suppressor role in NSCLC. Material and methods: The expression of FENDRR in NSCLC patients' tissues and cell line was detected by quantitative real-time PCR. MTT assay was used to detect cell proliferation and chemotherapy resistance. Cell apoptosis was measured by flow cytometry. Results: The expression of FENDRR was low in NSCLC tissues and cells in contrast to control tissues and cells, and low FENDRR expression correlated with high TNM stages and poor differentiation of NSCLC, and could be a promising prognostic factor for NSCLC. FENDRR enhancement could inhibit the proliferation ability and advance cell apoptosis of A549 cells. The expression of FENDRR in NSCLC tissues and cells insensitive to cisplatin was much lower than that in NSCLC tissues and cells sensitive to cisplatin. The chemotherapy resistance to cisplatin of A549/DDP cells was depressed by FENDRR enhancement, and IC50 for cisplatin presented a conspicuous depression. FENDRR up-regulation inhibited cell viability of A549/DDP cells under treatment with 5 μg/ml DDP. TCGA Pan-Cancer (PANCAN) showed that the expression of FENDRR was negatively correlated with the expression of ABCC10 in lung cancer, and our western blot found that FENDRR up-regulation inhibited the expression of ABCC10 in A549/DDP cells. Conclusions: LncRNA FENDRR has low expression in NSCLC and functions as a potential tumor-suppressing gene to inhibit growth and chemotherapy resistance of NSCLC cells.

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FOXM1 evokes 5-fluorouracil resistance in colorectal cancer depending on ABCC10

Cited by 65 publications

References 43 publications

Crosstalk between Nrf2 and YAP contributes to maintaining the antioxidant potential and chemoresistance in bladder cancer

Crosstalk between Nrf2 and YAP contributes to maintaining the antioxidant potential and chemoresistance in bladder cancer

5‐Fluorouracil resistance mechanisms in colorectal cancer: From classical pathways to promising processes

Long non-coding RNA FOXF1 adjacent non-coding developmental regulatory RNA inhibits growth and chemotherapy resistance in non-small cell lung cancer

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