Long noncoding RNA CASC2 promotes paclitaxel resistance in breast cancer through regulation of miR-18a-5p/CDK19

Zheng, Pengfei; Liu, Dong; Zhang, Bin; Dai, Jianli; Zhang, Yifu; Wang, Yanan; Qin, Shuang

doi:10.1007/s00418-019-01794-4

Cited by 51 publications

(33 citation statements)

References 33 publications

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“…Moreover, silenced CASC2 expression decreased DDP sensitivity in gastric cancer and cervical cancer [43,47]. Another study also revealed that upregulated CASC2 expression reduced the chemo-resistance of prostate cancer cells to docetaxel [48]. The results of this study were consistent with the above studies, suggesting that high CASC2 expression enhanced the chemo-sensitivity of DDP-resistant OSCC cells to DDP.…”

Section: Discussionsupporting

confidence: 89%

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Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1 axis

Wang

Jia

Zhou

2021

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Oral squamous cell cancer (OSCC) is a primary malignant tumor of the head and neck. Long non-coding RNA cancer susceptibility candidate 2 (CASC2) is related to the chemoresistance of diverse tumors. At present, the resistance of OSCC to first-line chemotherapy drug cisplatin (DDP) is still a giant problem. Herein, we investigated the role and mechanism of CASC2 in OSCC resistance to DDP. Expression levels of CASC2, miR-31-5p, and KANK1 in OSCC tissues and cells were determined by qRT-PCR. The half-maximal inhibitory concentration (IC50) value of DDP-resistant OSCC cells and apoptosis of DDP-resistant OSCC cells were determined via CCK-8 or flow cytometry assays. The relationship between CASC2 or KANK1 and miR-31-5p was verified with a dual-luciferase reporter or RIP assays. The role o f CASC2 in vivo was confirmed by xenograft experiments. We observed that CASC2A and KANK1 were downregulated while miR-31-5p was upregulated in DDP-resistant OSCC tissues and cells (p < 0.05). CASC2 overexpression enhanced cell DDP sensitivity and accelerated cell apoptosis in DDP-resistant OSCC cells in vivo and in vitro (p < 0.05). Notably, KANK1 acted as a target for miR-31-5p. Also, CASC2 modulated KANK1 expression via sponging miR-31-5p in DDP-resistant OSCC cells (p < 0.05). Both CASC2 and KANK1 introduction-mediated impacts on the DDP sensitivity and apoptosis of DDP-resistant OSCC cells were restored by miR-31-5p elevation (p < 0.05). To conclude, CASC2 boosted the DDP sensitivity and apoptosis of DDP-resistant OSCC cells by upregulating KANK1 via sponging miR-31-5p, and CASC2 might be a potential target for DDP-resistant OSCC treatment.

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Section: Discussionsupporting

confidence: 89%

“…The results of this study were consistent with the above studies, suggesting that high CASC2 expression enhanced the chemo-sensitivity of DDP-resistant OSCC cells to DDP. However, Zheng et al claimed that CASC2 reduced paclitaxel chemo-sensitivity in breast cancer, which might be related to the tissue specificity of CASC2 [48].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1 axis

Wang

Jia

Zhou

2021

neo

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“…Liu et al found that the upregulation of hsa_circ_0136666 promotes the progression of BC by spongifying miR-1299 and targeting CDK6 to inhibit the proliferation, migration, and invasion of BC [170]. Moreover, Zheng et al found that long non-coding RNA CASC2/miR-18a-5p/CDK19 is involved in BC chemical resistance [100] and the non-coding RNA 00511 (LINC00511)/miR-29c/CDK6 is involved in paclitaxel cytotoxicity in BC cells [171]. Taken together, these miRNAs can be used as candidate targets for novel CDK inhibitors in BC therapeutic purposes with miRNA antagonists (also called antagomirs or antimiRs, gene-silencing therapy) or miRNA mimics (also known as miRNA replacement therapy, replacement therapy).…”

Section: The Novel Cdk Inhibitors In Bcmentioning

confidence: 99%

The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer

Ding

Cao

Lin

et al. 2020

IJMS

341

216

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Cyclin-dependent kinases (CDKs) are serine/threonine kinases whose catalytic activities are regulated by interactions with cyclins and CDK inhibitors (CKIs). CDKs are key regulatory enzymes involved in cell proliferation through regulating cell-cycle checkpoints and transcriptional events in response to extracellular and intracellular signals. Not surprisingly, the dysregulation of CDKs is a hallmark of cancers, and inhibition of specific members is considered an attractive target in cancer therapy. In breast cancer (BC), dual CDK4/6 inhibitors, palbociclib, ribociclib, and abemaciclib, combined with other agents, were approved by the Food and Drug Administration (FDA) recently for the treatment of hormone receptor positive (HR+) advanced or metastatic breast cancer (A/MBC), as well as other sub-types of breast cancer. Furthermore, ongoing studies identified more selective CDK inhibitors as promising clinical targets. In this review, we focus on the roles of CDKs in driving cell-cycle progression, cell-cycle checkpoints, and transcriptional regulation, a highlight of dysregulated CDK activation in BC. We also discuss the most relevant CDK inhibitors currently in clinical BC trials, with special emphasis on CDK4/6 inhibitors used for the treatment of estrogen receptor-positive (ER+)/human epidermal growth factor 2-negative (HER2−) M/ABC patients, as well as more emerging precise therapeutic strategies, such as combination therapies and microRNA (miRNA) therapy.

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“…For example, lncRNA FTH1P3 was shown to expedite PTX resistance in BC via the miR-206/ABCB1 axis; 9 Han et al illuminated that lncRNA H19 activated PTX resistance in BC through inhibiting apoptosis and the regulation of Akt pathway; 10 Zheng et al asserted that CASC2 generated the promotion of PTX resistance of BC by regulating miR-18a-5p/CDK19. 11 Recently, urothelial carcinoma-associated 1 (UCA1) was reported to be dysregulated in BC and involved in the multiple resistance regulation. 12 But the role and functional mechanism of UCA1 in PTX resistance in BC are obscure.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis</p>

Liu¹,

Jiang²,

Zhang³

et al. 2020

CMAR

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Background: Paclitaxel (PTX) occupies a considerable status in the chemotherapies of breast cancer (BC), but the drug resistance keeps an obstructive factor of PTX treatment. This study was designed to explore the molecular mechanism of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) in PTX resistance of BC. Methods: UCA1, microRNA-613 (miR-613) and cyclin-dependent kinase 12 (CDK12) expression was assayed through quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay was implemented for evaluating the half inhibitory concentrations (IC 50) of PTX and cell viability. Cell apoptosis was examined by flow cytometry. The target relationship was explored using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CDK12 protein level was detected through Western blot. Xenograft tumor assay was applied for assessing the influence of UCA1 on PTX resistance of BC in vivo. Results: UCA1 expressed highly in PTX-resistant BC tissues and cells and regulated PTX resistance in BC cells by affecting cell viability and apoptosis in part. UCA1 negatively interacted with miR-613 and modulated PTX resistance via sponging miR-613. CDK12 was a downstream gene of miR-613 and miR-613 exerted the modulation of PTX resistance via targeting CDK12. Furthermore, UCA1 regulated CDK12 level through interacting with miR-613. The regulatory role of UCA1 in PTX resistance of BC was achieved by miR-613/ CDK12 axis in vivo. Conclusion: UCA1 mediated PTX resistance in BC through the miR-613/CDK12 axis, manifesting that UCA1 might improve the PTX treatment of BC as a significant therapeutic biomarker.

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Long noncoding RNA CASC2 promotes paclitaxel resistance in breast cancer through regulation of miR-18a-5p/CDK19

Cited by 51 publications

References 33 publications

Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1 axis

Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1 axis

The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer

<p>Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis</p>

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