Screening of molecular targets and construction of a ceRNA network for oxaliplatin resistance in colorectal cancer

Wu, Wei; Xi, Yang; Xu, Jingying; Jing, Zhuang; Han, Shuwen

doi:10.1039/c9ra06146k

Cited by 5 publications

(4 citation statements)

References 48 publications

(33 reference statements)

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“…Previous studies demonstrated that HOTAIR enhanced the resistance of colorectal cancer to oxaliplatin 15–17 . To our knowledge, for the first time our evidence demonstrated that HOTAIR contributed to the resistance of GC to oxaliplatin dependent on ABCG2.…”

Section: Discussionsupporting

confidence: 58%

“…Previous studies demonstrated that HOTAIR enhanced the resistance of colorectal cancer to oxaliplatin. [15][16][17] To our knowledge, for the first time our evidence demonstrated that HOTAIR contributed to the resistance of GC to oxaliplatin dependent on ABCG2. These evidences indicated that HOTAIR could be a promising target for personalization chemotherapy for GC in future.…”

Section: Discussionmentioning

confidence: 60%

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Dampening HOTAIR sensitizes the gastric cancer cells to oxaliplatin through miR‐195‐5p and ABCG2 pathway

Luo,

Lu,

et al. 2023

J Cellular Molecular Medi

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Long non‐coding RNAs (lncRNA) have an extensive role in the progression and chemoresistance of gastric cancer (GC). Deeply study the regulatory role of lncRNAs could provide potential therapeutic targets. The aim of this study is to explore the regulatory role of HOTAIR in the progression and oxaliplatin resistance of GC. The expression of HOTAIR in GC and cell lines were detected by using qRT‐PCR. Cell proliferation and apoptosis were analysed by CCK‐8, EdU incorporation and flow cytometry. Luciferase reporter assay was used to identify the interaction between HOTAIR and ABCG2 (ATP‐binding cassette (ABC) superfamily G member 2, ABCG2) via miR‐195‐5p. The regulatory functions were verified by using molecular biology experiments. HOTAIR was significantly overexpressed in GC and associated with poor prognosis. Knock‐down of HOTAIR inhibited the GC cells proliferation and oxaliplatin resistance, while overexpression of HOTAIR showed opposite functions. Further studies found that HOTAIR acted as a competing endogenous RNA (ceRNA) to absorb miR‐195‐5p and elevated the expression of ABCG2, which leads to resistance of GC cells to oxaliplatin. Taken together, our findings demonstrated that HOTAIR regulates ABCG2 induced resistance of GC to oxaliplatin through miR‐195‐5p signalling and illustrate the great potential of developing new therapeutic targets for GC patients.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 60%

Dampening HOTAIR sensitizes the gastric cancer cells to oxaliplatin through miR‐195‐5p and ABCG2 pathway

Luo,

Lu,

et al. 2023

J Cellular Molecular Medi

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“…Specifically, the ceRNA network developed by the authors contained 503 lncRNA-miRNA-mRNA regulatory, 210 lncRNA-miRNA pairs, 382 miRNA-mRNA, and 212 mRNA co-expression pairs. Among these, HOTAIR and 14 mRNAs significantly correlated with patient prognosis for oxaliplatin resistance ( Wei et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

The role of HOTAIR in the modulation of resistance to anticancer therapy

Cantile,

Belli,

Scognamiglio

et al. 2024

Front. Mol. Biosci.

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Leading anti-tumour therapeutic strategies typically involve surgery and radiotherapy for locally advanced (non-metastatic) cancers, while hormone therapy, chemotherapy, and molecular targeted therapy are the current treatment options for metastatic cancer. Despite the initially high sensitivity rate to anticancer therapies, a large number of patients develop resistance, leading to a poor prognosis. The mechanisms related to drug resistance are highly complex, and long non-coding RNAs appear to play a crucial role in these processes. Among these, the lncRNA homeobox transcript antisense intergenic RNA (HOTAIR), widely implicated in cancer initiation and progression, likewise plays a significant role in anticancer drug resistance. It can modulate cell activities such as proliferation, apoptosis, hypoxia, autophagy, as well as epithelial-mesenchymal transition, thereby contributing to the development of resistant tumour cells. In this manuscript, we describe different mechanisms of antitumor drug resistance in which HOTAIR is involved and suggest its potential as a therapeutic predictive biomarker for the management of cancer patients.

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“…MiRNA are involved in important life processes such as cell proliferation and apoptosis, gene expression regulation, and individual development [14]. miRNA is closely related to tumorigenesis, development, and resistance to chemotherapy [15]. MiR-503-3p is a newly discovered mi RNA that is involved in the proliferation of certain tumors [16].…”

Section: Introductionmentioning

confidence: 99%

circBIRC6 regulates cisplatin resistance of choroidal melanoma via positively modulating ERK by sponging miR-503-3p

Nie

Jin

et al. 2020

Preprint

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Background/AimscircRNA plays a key regulatory role in various human tumors. This study was carried out to investigate the molecular mechanism of circBIRC6 in the regulation of choroidal melanoma cisplatin (DDP) resistance. MethodsThe expression of circBIRC6 in choroidal melanoma tissues and cells (MUM-2B, MUM-2B / DDP) was detected by RT-qPCR. The function of circBIRC6 in DDP resistance of choroidal melanoma was analyzed by functional loss and overexpression experiments. DDP inhibition rate was detected by MTT method. Western blot was used to analysis the protein levels of P-gp, MRP1 and ERK. The relationship between circBIRC6, miR-503-3p and ERK was analyzed by CircRIP and luciferase reporter vector assay.ResultcircBIRC6 was up-regulated in choroidal melanoma, and it was significantly raised in choroidal melanoma tissues and cells that are resistant to DDP. CircBIRC6 regulated DDP resistance of choroidal melanoma cells by binding to miR-503-3p. ERK was directly targeted by miR-503-3p, and ERK inhibited miR-503-3p-induced DDP resistance. Finally, the expression of circBIRC6 was positively correlated with ERK, and it was verified that circBIRC6 regulated ERK by targeting miR-503-3p.ConclusionCircBIRC6 regulated the expression of ERK choroidal melanoma cells and DDP resistance via miR-503-3p. These results suggested that the knockout of circBIRC6 may provide an effective treatment strategy for choroidal melanoma.

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Screening of molecular targets and construction of a ceRNA network for oxaliplatin resistance in colorectal cancer

Abstract: Oxaliplatin resistance reduces the efficacy of chemotherapy for colorectal cancer (CRC).

Cited by 5 publications

References 48 publications

Dampening HOTAIR sensitizes the gastric cancer cells to oxaliplatin through miR‐195‐5p and ABCG2 pathway

Dampening HOTAIR sensitizes the gastric cancer cells to oxaliplatin through miR‐195‐5p and ABCG2 pathway

The role of HOTAIR in the modulation of resistance to anticancer therapy

circBIRC6 regulates cisplatin resistance of choroidal melanoma via positively modulating ERK by sponging miR-503-3p

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