&lt;p&gt;Knockdown of lncRNA &lt;em&gt;PCAT6&lt;/em&gt; Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating&lt;em&gt; miR-185-5p&lt;/em&gt;/&lt;em&gt;TPD52&lt;/em&gt; Axis&lt;/p&gt;

Shi, Rui; Wu, Peng; Liu, Miaomiao; Chen, Bing; Cong, Longjiao

doi:10.2147/ott.s237559

Cited by 38 publications

(34 citation statements)

References 45 publications

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“…Lv et al (40) showed that PCAT6-overexpression promotes cell proliferation, migration, invasion and reduces apoptosis through the activation of the Wnt/β-catenin pathway in cervical cancer. Other studies have demonstrated that knockdown of PCAT6 reverses chemoresistance of cancer cells to 5-fluorouracil and enhances radiosensitivity in breast cancer cells (41,42). The aforementioned results of the present study indicated that the oncogene PCAT6 might be an effective therapeutic target for patients with liver cancer.…”

Section: Discussionsupporting

confidence: 74%

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

et al. 2021

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Liver cancer is one of the most common malignant human tumors with the highest morbidity and mortality rates of all cancer types in China. Evidence suggests that long non-coding RNA prostate cancer-associated transcript 6 (PCAT6) plays an essential role in tumor progression. However, the roles and mechanism of PCAT6 in liver cancer remain unclear. The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. Moreover, knockdown of PCAT6 significantly inhibited the proliferation and invasion of liver cancer cells in vitro and in vivo. A dual-luciferase reporter gene assay demonstrated that PCAT6 could bind to miR-326 and that hnRNPA2B1 was a direct target gene of miR-326. Mechanistically, silenced PCAT6 suppressed the malignant phenotype of liver cancer cells through upregulating the inhibitory effect of miR-326 on hnRNPA2B1 expression. Taken together, these data demonstrated that knockdown of PCAT6 inhibited liver cancer progression through regulation of the miR-326/hnRNPA2B1 axis, suggesting that PCAT6 functions as an oncogene and may be a useful biomarker for the future diagnosis and treatment of liver cancer.

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Section: Discussionsupporting

confidence: 74%

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

et al. 2021

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“…Our data show several lncRNAs to be upregulated in persistence cells in comparison to those in the extinction group (CBR3-AS1, RGPD4-AS1, AL356608.1, KCNMA1-AS1, SOX2-OT, LYPLAL1-AS1, AC068831.7, TMEM254-AS1, AC015849.12, and AC015849.3). Countless other studies have associated different lncRNAs to TNBC regulation, progression and even radio-sensitivity 15,[20][21][22][23] , establishing the oncogenic potential of some lncRNAs, which can serve as targets for therapeutic intervention against TNBC.…”

Section: Discussionmentioning

confidence: 99%

Single-cell long noncoding RNA (lncRNA) transcriptome implicates MALAT1 in triple-negative breast cancer (TNBC) resistance to neoadjuvant chemotherapy

et al. 2021

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Cumulative evidence suggests added benefit for neoadjuvant chemotherapy (NAC) in a subset of triple-negative breast cancer (TNBC) patients. Herein we identified the long noncoding RNA (lncRNA) transcriptional landscape associated with TNBC resistance to NAC, employing 1758 single cells from three extinction and three persistence TNBC patients. Using Iterative Clustering and Guide-gene Selection (ICGS) and uniform manifold approximation and projection (UMAP) dimensionality reduction analysis, we observed single cells derived from each patient to largely cluster together. Comparing the lncRNA transcriptome from single cells through the course of NAC treatment revealed minimal overlap based on lncRNA transcriptome, suggesting substantial effects of NAC on lncRNA transcription. The differential analysis revealed upregulation of 202 and downregulation of 19 lncRNAs in the persistence group, including upregulation of five different transcripts encoding for the MALAT1 lncRNA. CRISPR/Cas9-mediated MALAT1 promoter deletion in BT-549 TNBC model enhanced sensitivity to paclitaxel and doxorubicin, suggesting a role for MALAT1 in conferring resistance. Mechanistically, whole transcriptome analysis of MALAT1-KO cells revealed multiple affected mechanistic networks as well as oxidative phosphorylation canonical and angiogenesis functional category. Interestingly, lncRNA profiling of MALAT1-depleted TNBC also revealed a number of altered lncRNAs in response to MALAT1 deletion, suggesting a reciprocal relationship between MALAT1 and a number of lncRNAs, including NEAT1, USP3-AS1, and LINC-PINT, in TNBC. Elevated expression of MALAT1, USP3-AS1, and LINC-PINT correlated with worse clinical outcomes in BC patients. Our data revealed the lncRNA transactional portrait and highlighted a complex regulatory network orchestrated by MALAT1 in the context of TNBC resistance to NAC therapy.

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“…Importantly, blocking LINP1 could increase the sensitivity of the tumour‐cell response to radiotherapy in TNBC 117 . Additionally, knockdown of lncRNA PCAT6 promoted the radiosensitivity of TNBC cells through regulating miR‐185‐5p/TPD52 axis 118 . Taken together, these studies evoke the potential of altering lncRNAs expression in future to represent a novel therapeutic approach to reverse drug resistance or radiotherapy resistance in TNBC patients.…”

Section: Roles Of Lncrnas In Tnbcmentioning

confidence: 81%

The long non‐coding RNA landscape in triple‐negative breast cancer

2020

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Breast cancer (BC) is the most frequently diagnosed malignancy and the leading cause of cancer death in females worldwide. 1 Triple-negative breast cancer (TNBC) is a subgroup of breast cancers that lack the expression of oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER-2). 2 The risk of distant recurrence and metastasis in TNBC patients is substantially higher than in non-TNBC patients. 3 The clinical management of TNBC is challenging because of the relatively aggressive biologic behaviour and paucity of specific targeted therapy. 4 Thus, a better understanding of the regulations and mechanisms of tumorigenesis in TNBC cells and the identification of effective biomarkers for diagnosis and prognosis of TNBC patients are consequently keenly awaited. LncRNAs, with a length exceeding 200 nucleotides, are non-protein-coding transcripts. 5 Accumulating studies report that lncRNAs expression is dysregulated in various types of cancer

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<p>Knockdown of lncRNA <em>PCAT6</em> Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating<em> miR-185-5p</em>/<em>TPD52</em> Axis</p>

Cited by 38 publications

References 45 publications

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

Single-cell long noncoding RNA (lncRNA) transcriptome implicates MALAT1 in triple-negative breast cancer (TNBC) resistance to neoadjuvant chemotherapy

The long non‐coding RNA landscape in triple‐negative breast cancer

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