Long Noncoding RNAs as Biotargets in Cisplatin-Based Drug Resistance

Abu, Nadiah; Hon, Kha Wai; Jeyaraman, Shivapriya; Jamal, A. Rahman A.

doi:10.2217/fon-2018-0303

Cited by 27 publications

(23 citation statements)

References 84 publications

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“…[8][9][10] Moreover, dysregulated lncRNAs have been reported to be implicated with cisplatin resistance in various cancers. 11 LncRNA small nucleolar RNA host gene 15 (SNHG15), an intergenic lncRNA located on chromosome 7p13, belongs to a family of non-coding RNAs that hosting snoRNAs. 12 Previous studies suggest that SNHG15 could promote cancer cell proliferation and invasiveness and is able to play as a crucial determinant role in the chemoresistance.…”

Section: Introductionmentioning

confidence: 99%

SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381

Mi¹,

Wang²,

Wang³

et al. 2020

OTT

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Background: Increasing evidence implies the participation of long non-coding RNAs (lncRNAs) in chemoresistance to cancer treatment. Their role and molecular mechanisms in breast cancer chemoresistance, nevertheless, are yet not considerably elucidated. In this work, we research the function of small nucleolar RNA host gene 15 (SNHG15) in cisplatin (DDP) resistance of breast cancer and uncover the underlying molecular mechanism. Methods: SNHG15 and miR-381 expression levels were detected using Quantitative realtime PCR (qRT-PCR) analysis. The functional roles of SNHG15 and miR-381 in breast cancer were determined using MTT assay and flow cytometry analysis. The effect of SNHG15 on miR-381 expression was determined using Luciferase reporter assay, RNA immunoprecipitation (RIP) assay and qRT-PCR analysis. Results: SNHG15 was found to be up-regulated in cisplatin resistant breast cancer tissues and cell lines. Breast cancer patients with high SNHG15 expression had a poor prognosis. SNHG15 silencing enhanced cisplatin sensitivity of MCF-7/DDP and MDA-MB-231/DDP cells. Additionally, SNHG15 could function as a miR-381 sponge. miR-381 overexpression could overcome cisplatin resistance. miR-381 knockdown countered SNHG15 knockdown-mediated enhancement of cisplatin sensitivity in MCF-7/DDP and MDA-MB-231/DDP cells. Besides, SNHG15 knockdown facilitated cisplatin sensitivity of cisplatin resistant breast cancer cells in vivo. Conclusion: In summary, SNHG15 knockdown overcame cisplatin resistance of breast cancer by sponging miR-381, providing a novel therapeutic target for breast cancer.

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Section: Introductionmentioning

confidence: 99%

SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381

Mi¹,

Wang²,

Wang³

et al. 2020

OTT

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show abstract

“…In addition, hypoxia, epithelial-mesenchymal transition, apoptosis inhibition and changes in molecular signalling pathways also contribute to drug resistance 10 . Studies have suggested that cisplatin resistance is related to regulation of the cell cycle, apoptosis and the Wnt pathway by long non-coding RNAs (lncRNAs) 11 . LncRNAs are small non-coding RNAs with more than 200 nucleotides and account for 80% of all non-coding RNAs.…”

Section: Introductionmentioning

confidence: 99%

Low GAS5 expression may predict poor survival and cisplatin resistance in cervical cancer

et al. 2020

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Cisplatin resistance is a major challenge in cervical cancer (CC) chemotherapy. Growth arrest‐specific 5 (GAS5) has been reported to be a tumour suppressor gene in CC. However, the mechanism of GAS5 in chemoresistance remains undetermined. Our research evaluated GAS5 expression in normal and CC tissues by qPCR and in situ hybridization (ISH). Statistical analysis was conducted to analyse the association of GAS5 expression with survival. Biochemical methods were used to screen upstream and downstream regulators of GAS5. Then, interactions were confirmed by ChIP, RNA pull-down, RNA immunoprecipitation (RIP), dual-luciferase reporter and real-time PCR assays. The cisplatin sensitivity of GAS5-overexpressing CC cells was demonstrated in vitro and in vivo. The results showed that low GAS5 expression was correlated with poor overall survival. Mechanistically, GAS5 was transcriptionally modulated by P-STAT3 and served as a competing endogenous RNA (ceRNA) of miR-21 to indirectly affect cisplatin sensitivity through PDCD4 regulation in CC cells. Animal studies confirmed that GAS5 enhanced cisplatin sensitivity and promoted PDCD4 expression in vivo. GAS5 was regulated by P-STAT3 and affected the sensitivity of CC to cisplatin-based chemotherapy through the miR-21/PDCD4 axis. This result may provide new insight into cisplatin-based therapy.

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“…25,26 LncRNAs played important roles in the regulation of tumorigenesis and drug resistance in ovarian cancer. 27,28 Previous studies demonstrated that NEAT1 acted as an oncogenic lncRNA to promote the progression of ovarian cancer. 7,10 However, whether NEAT1 could regulate cisplatin resistance in ovarian cancer remains unclear.…”

Section: Discussionmentioning

confidence: 99%

NEAT1 Knockdown Suppresses the Cisplatin Resistance in Ovarian Cancer by Regulating miR-770-5p/PARP1 Axis

Zhu¹,

Yang²,

Wang³

2020

CMAR

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Background: Long noncoding RNAs play essential roles in regulating drug resistance in cancers. However, how and whether lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) could mediate cisplatin resistance in ovarian cancer remain poorly understood. Patients and Methods: Eighteen cisplatin-sensitive and 19 cisplatin-resistant patients with ovarian cancer were recruited. Cisplatin-resistant ovarian cancer cells were used for this study. The expression levels of NEAT1, microRNA (miR)-770-5p and poly adenosine diphosphate-ribose polymerase 1 (PARP1) were detected by quantitative real-time polymerase chain reaction or Western blot. Cisplatin resistance was assessed by the half-maximal inhibitory concentration (IC50) of cisplatin, cell viability and apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, flow cytometry and Western blot, respectively. The target association between miR-770-5p and NEAT1 or PARP1 was investigated by dual-luciferase reporter assay. The xenograft model was used to investigate cisplatin resistance in vivo. Results: NEAT1 expression is elevated in cisplatin-resistant ovarian cancer tissues and cells. Knockdown of NEAT1 repressed cisplatin resistance by decreasing the IC50 of cisplatin, cell viability and increasing apoptosis. MiR-770-5p was bound to NEAT1 and PARP1 was confirmed as a target of miR-770-5p. MiR-770-5p inhibition or PARP1 restoration could abate the effect of NEAT1 silencing on cisplatin resistance in cisplatin-resistant ovarian cancer cells. Moreover, NEAT1 knockdown reduced PARP1 expression by increasing miR-770-5p. Interference of NEAT1 decreased xenograft tumor growth by regulating miR-770-5p and PARP1. Conclusion: Knockdown of NEAT1 inhibited cisplatin resistance in ovarian cancer cells by up-regulating miR-770-5p and down-regulating PARP1, providing a new target for improving the efficacy of cisplatin-based therapy in ovarian cancer.

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Long Noncoding RNAs as Biotargets in Cisplatin-Based Drug Resistance

Cited by 27 publications

References 84 publications

<p>SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381</p>

<p>SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381</p>

Low GAS5 expression may predict poor survival and cisplatin resistance in cervical cancer

<p>NEAT1 Knockdown Suppresses the Cisplatin Resistance in Ovarian Cancer by Regulating miR-770-5p/PARP1 Axis</p>

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