Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression

Hang, Qun; Sun, Ruochuan; Jiang, Congqiao; Li, Yongxiang

doi:10.1097/cad.0000000000000227

Cited by 72 publications

(43 citation statements)

References 25 publications

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“…Zhang et al showed that lncRNA plasmacytoma variant translocation-1 (PVT-1) was highly expressed in gastric cancer tissues from cisplatin-resistant patients and cisplatin-resistant gastric cancer cells; and overexpression of PVT1 in gastric carcinoma promoted the development of MDR (42). Furthermore, Hang et al demonstrated that high expression of lncRNA AK022798 induced by Notch1 resulted in the formation of cisplatin-resistant SGC7901 and BGC823 cells via regulating the expression of ABCC1 and ABCB1 (43). The current study utilized the overexpression of NEAT1 in K562 and THP-1 cell lines to determine the MDR function in response to two different anti-leukemic drugs.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of lncRNA NEAT1 mitigates multidrug resistance by inhibiting ABCG2 in leukemia

et al. 2016

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Abstract. Leukemia is a heterogeneous clonal disorder in which early hematopoietic cells fail to differentiate and do not undergo programmed cell death or apoptosis. Less than one-third of adult patients with leukemia are managed using current therapies due to the emergence of multidrug resistance (MDR), emphasizing the need for newer and more robust approaches. Recent reports have suggested that long non-coding RNAs (lncRNAs) contribute to selective gene expression and, hence, could be manipulated effectively to halt the progression of cancer. However, little is known regarding the role of lncRNA in leukemia. Nuclear paraspeckle assembly transcript 1 (NEAT1) is a nuclear-restricted lncRNA involved in the pathogenesis of certain types of cancer. Deregulated expression of NEAT1 has been reported in a number of human malignancies, including leukemia and other solid tumors. The present study aimed to characterize the role of NEAT1 in the regulation of MDR in leukemia. Using reverse transcription-quantitative polymerase chain reaction, it was demonstrated that NEAT1 messenger RNA (mRNA) expression levels were significantly downregulated in leukemia patient samples compared with those from healthy donors. Furthermore, NEAT1 mRNA expression was repressed in a number of leukemia cell lines, including K562, THP-1, HL-60 and Jurkat cells, compared with peripheral white blood control cells, consistent with the expression observed in patients with leukemia. In addition, the transfection of a NEAT1 overexpression plasmid into K562 and THP-1 leukemia cell lines alleviated MDR induced by cytotoxic agents, such as Alisertib and Bortezomib, through inhibition of ATP-binding cassette G2. Although more robust studies are warranted, the current findings provide the basis for the use of NEAT1 as a novel promising target in the treatment of leukemia.

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Section: Discussionmentioning

confidence: 99%

Overexpression of lncRNA NEAT1 mitigates multidrug resistance by inhibiting ABCG2 in leukemia

et al. 2016

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“…This previous study also suggested that Notch1 is significantly upregulated in SGC7901/DDP and BGC823/DDP cells (85). The activation of Notch1 via transfection of the Notch1 overexpression vector plasmid may promote lncRNA AK022798 expression and increase the expression of MRP1, P-glycoprotein, and reduce the apoptosis of SGC7901 and BGC823 cells (85). The results of this previous study suggest that Notch1 may promote cisplatin-resistant gastric cancer formation and inhibit apoptosis, at least partially through upregulating the expression of lncRNA AK022798 (85), whilst the regulation mechanism remains unclear.…”

Section: Gastric Cancermentioning

confidence: 65%

Section: Gastric Cancermentioning

confidence: 92%

“…The lncRNA AK022798 is upregulated in gastric cancer and serves important functions in tumorigenesis, as a previous study suggested (85). The silencing of lncRNA AK022798 by specific siRNAs not only decreases the expression of multidrug resistance-associated protein 1 (MRP1) and P-glycoprotein, but also enhances the apoptotic activity of certain cisplatin-resistant gastric cancer cell lines (including SGC7901/DDP and BGC823/DDP cell lines) (85).…”

Section: Gastric Cancermentioning

confidence: 97%

“…The silencing of lncRNA AK022798 by specific siRNAs not only decreases the expression of multidrug resistance-associated protein 1 (MRP1) and P-glycoprotein, but also enhances the apoptotic activity of certain cisplatin-resistant gastric cancer cell lines (including SGC7901/DDP and BGC823/DDP cell lines) (85). This previous study also suggested that Notch1 is significantly upregulated in SGC7901/DDP and BGC823/DDP cells (85). The activation of Notch1 via transfection of the Notch1 overexpression vector plasmid may promote lncRNA AK022798 expression and increase the expression of MRP1, P-glycoprotein, and reduce the apoptosis of SGC7901 and BGC823 cells (85).…”

Section: Gastric Cancermentioning

confidence: 99%

See 2 more Smart Citations

Crosstalk between the Notch signaling pathway and non‑coding RNAs in gastrointestinal cancers (Review)

2017

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Abstract. The Notch signaling pathway is one of the main signaling pathways that mediates direct contact between cells, and is essential for normal development. It regulates various cellular processes, including cell proliferation, apoptosis, migration, invasion, angiogenesis and metastasis. It additionally serves an important function in tumor progression. Non-coding RNAs mainly include small microRNAs, long non-coding RNAs and circular RNAs. At present, a large body of literature supports the biological significance of non-coding RNAs in tumor progression. It is also becoming increasingly evident that cross-talk exists between Notch signaling and non-coding RNAs. The present review summarizes the current knowledge of Notch-mediated gastrointestinal cancer cell processes, and the effect of the crosstalk between the three major types of non-coding RNAs and the Notch signaling pathway on the fate of gastrointestinal cancer cells.

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Hypermethylation of lncRNA MEG3 impairs chemosensitivity of breast cancer cells

Wang

Liu

et al. 2020

Clinical Laboratory Analysis

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Background Chemoresistance posed a barrier to successful treatment of breast cancer (BC), and lncRNA MEG3 has been documented to implicate in BC development. However, whether MEG3 methylation, which led to low MEG3 expression, was relevant to BC progression and chemoresistance remained uncertain. Methods In the aggregate, 374 pairs of tumor tissues and adjacent normal tissues were collected from pathologically confirmed BC patients, and four BC cell lines, including MDA‐MB‐231, Bcap‐37, MCF‐7, and SK‐BR‐3, were purchased. Moreover, methylation‐specific polymerase chain reaction (PCR) was adopted to evaluate the methylation status of BC tissues and cell lines, and chemo‐tolerance of BC cell lines was assessed by performing MTT assay. Concurrently, transwell assay and scratch assay were carried out to estimate the migratory and invasive capability of BC cell lines. Results Methylated MEG3, lowly expressed MEG3, large tumor size (≥2 cm), advanced TNM grade and lymphatic metastasis were potentially symbolic of poor prognosis among BC patients (P < .05). Besides, MDA‐MB‐231 cell line exhibited the strongest resistance against paclitaxel, adriamycin, and vinorelbine (P < .05), while MCF‐7 cell line seemed more sensitive against these drugs than any other BC cell line (P < .05). Furthermore, pcDNA3.1‐MEG3 and 5‐Aza‐dC markedly sensitized MDA‐MB‐231 and MCF‐7 cell lines against the drug treatments (P < .05). Simultaneously, proliferation and metastasis of the BC cell lines were slowed down under the force of pcDNA3.1‐MEG3 and 5‐Aza‐dC (P < .05). Conclusion Preventing methylation of MEG3 might matter in lessening BC chemoresistance, owing to its hindering proliferation and metastasis of BC cells.

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Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression

Cited by 72 publications

References 25 publications

Overexpression of lncRNA NEAT1 mitigates multidrug resistance by inhibiting ABCG2 in leukemia

Overexpression of lncRNA NEAT1 mitigates multidrug resistance by inhibiting ABCG2 in leukemia

Crosstalk between the Notch signaling pathway and non‑coding RNAs in gastrointestinal cancers (Review)

Hypermethylation of lncRNA MEG3 impairs chemosensitivity of breast cancer cells

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