The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer

Xing, Zengshu; Li, Sailian; Liu, Zhenxiang; Zhang, Chong; Meng, Meijiang; Bai, Zhiming

doi:10.1042/bsr20191850

Cited by 25 publications

(13 citation statements)

References 31 publications

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“…Meanwhile, our results illustrated that miR-195-5p was poorly expressed in prostate cancer and that its upregulation could repress prostate cancer cell proliferation, migration and invasion. Consistently, previous research has also indicated that prostate cancer cells exhibit poor expression of miR-195-5p, and that its upregulation limits cancer cell proliferation (Xing et al, 2020). The overexpression of miR-195 has been reported to markedly suppress prostate cancer cell proliferation and tube formation by downregulating proline-rich protein 11 (PRR11) expression (Cai et al, 2018).…”

Section: Discussionsupporting

confidence: 59%

Long Non-coding RNA AGAP2-AS1 Silencing Inhibits PDLIM5 Expression Impeding Prostate Cancer Progression via Up-Regulation of MicroRNA-195-5p

et al. 2020

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Prostate cancer remains a significant cause of cancer-related deaths in male population. More recently, accumulating evidence continues to implicate long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs in various types of cancers, including prostate cancer. The current study aimed to elucidate the role of lncRNA AGAP2-AS1/miR-195-5p/PDZ and LIM domain 5 (PDLIM5) in prostate cancer progression. Initially, microarray expression profiles were applied to screen differentially expressed lncRNAs/miRNAs/genes associated with prostate cancer. Dual-luciferase reporter and RNA pull-down/RIP assays were subsequently performed to explore the interactions among lncRNA AGAP2-AS1, miR-195-5p, and PDLIM5, after which their expression was detected in cancer tissues and cells. Next, gain-and loss-of-function approaches were employed to elucidate the mechanism of lncRNA AGAP2-AS1/miR-195-5p/PDLIM5 in the processes of cell proliferation, migration and invasion as well as tumor growth. LncRNA AGAP2-AS1 was found to be highly expressed in prostate cancer. Silencing of lncRNA AGAP2-AS1 contributed to the suppression of proliferation, migration and invasion of cancer cells in vitro. Besides, lncRNA AGAP2-AS1 could bind to miR-195-5p which targeted PDLIM5 and subsequently downregulated its expression, ultimately impeding the progression of prostate cancer. Additionally, lncRNA AGAP2-AS1 inhibition led to an up-regulated expression of miR-195-5p and down-regulated PDLIM5 expression, resulting in delayed tumor growth in vivo. Taken together, the key findings of our study demonstrated that lncRNA AGAP2-AS1 silencing exerted suppressive effects on the development of prostate cancer via the miR-195-5pdependent downregulation of PDLIM5. Our findings highlighted the potential of lncRNA AGAP2-AS1 as a promising novel molecular target for prostate cancer therapy.

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Section: Discussionsupporting

confidence: 59%

Long Non-coding RNA AGAP2-AS1 Silencing Inhibits PDLIM5 Expression Impeding Prostate Cancer Progression via Up-Regulation of MicroRNA-195-5p

et al. 2020

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“…Previous data suggest that SEPT2 acts as an oncogene to facilitate the development of multiple cancers, 35,36 but its role in regulating LSCC pathogenesis has not been investigated. Given that SEPT2 is significantly upregulated in both LSCC tissues and cells (Figure 1A–I), we hypothesize that SEPT2 may also promote LSCC development.…”

Section: Resultsmentioning

confidence: 99%

The LncRNA FGD5‐AS1/miR‐497‐5p axis regulates septin 2 (SEPT2) to accelerate cancer progression and increase cisplatin‐resistance in laryngeal squamous cell carcinoma

Song

Zhang

et al. 2021

Molecular Carcinogenesis

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Aberrant expression or mutation of the Septin gene family is closely associated with cancer progression, and septin 2 (SEPT2) exerts its tumor‐promoting effects in multiple cancers, but its role in regulating laryngeal squamous cell carcinoma (LSCC) progression and drug resistance has not been investigated. Based on the published data, the present study identified that SEPT2 promoted cancer progression and increased cisplatin‐resistance in LSCC, and a novel LncRNA FGD5‐AS1/miR‐497‐5p axis was crucial for this process. Mechanistically, SEPT2 tended to be enriched in LSCC tissues and cells, and knock‐down of SEPT2 inhibited cell proliferation, viability, migration, and tumorigenesis in LSCC cells in vitro and in vivo. Aside from that, SEPT2 overexpression increased cisplatin resistance in LSCC cells. Next, by conducting the dual‐luciferase reporter gene system assay, we identified that the LncRNA FGD5‐AS1/miR‐497‐5p axis regulated SEPT2 in LSCC. Specifically, LncRNA FGD5‐AS1 sponged miR‐497‐5p to upregulate SEPT2 in LSCC cells in a competing endogenous RNA (ceRNA) mechanisms‐dependent manner. Interestingly, upregulated LncRNA FGD5‐AS1 and downregulated miR‐497‐5p were observed in LSCC tissues and cells, and LncRNA FGD5‐AS1 ablation inhibited cancer progression. Also, LncRNA FGD5‐AS1 overexpression increased cisplatin‐resistance in LSCC by modulating the miR‐497‐5p/SEPT2 axis. Collectively, we conclude that targeting the LncRNA FGD5‐AS1/miR‐497‐5p/SEPT2 signaling cascade may be an alternative strategy to treat LSCC in the clinic.

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“…Our findings demonstrated that LINC00473 Furthermore, Xing et al reported that LINC00473 promoted the proliferation of prostate cancer cells via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis. 12) In another study of Bai et al, LINC00473…”

Section: Discussionmentioning

confidence: 97%

Knockdown of Long Non-coding RNA LINC00473 Protects CHON-001 Cells against Interleukin-1β-Induced Cell Injury

Ding

Tong

et al. 2021

Biological & Pharmaceutical Bulletin

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Osteoarthritis is a chronic joint disease with high prevalence. However, effective treatment options for OA are still lacking. It was previously reported that LINC00473 was upregulated in patients with OA and upregulated LINC00473 might associated with the progression of OA; however, the role of LINC00473 in OA remains to be investigated. CHON-001 human chondrocyte cells stimulated with 10 ng/ml IL-1β were utilized to mimic OA in vitro. Protein expression, cell apoptosis and cell proliferation of CHON-001 cells were investigated by western blot, Annexin V and PI double staining, cell counting-8 kit assay and immunofluorescence staining respectively. The result indicated IL-1β triggered viability decrease and apoptosis in CHON-001 cells, which was alleviated by LINC00473 knockdown. Meanwhile, IL-1β-induced upregulation of cleaved caspase 3 and Bax were ameliorated by LINC00473 knockdown. Likewise, IL-1β-induced downregulation of XIAP was alleviated by LINC00473 knockdown. In addition, LINC00473 knockdown protected CHON-001 cells against IL-1β by inhibiting the methylation of LIM mineralization protein-1 (LMP)-1 gene. Moreover, JNK/NF-κB signaling pathway was proved to be involved in the cell protective effect of LINC00473 knockdown in IL-1β treated CHON-001 cells. Taken together, LINC00473 knockdown defended CHON-001 cells from IL-1β induced cell injury via inhibition of the methylation of LMP-1. Thus, LINC00473 might possibly act as a novel therapeutic target for OA.

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The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer

Cited by 25 publications

References 31 publications

Long Non-coding RNA AGAP2-AS1 Silencing Inhibits PDLIM5 Expression Impeding Prostate Cancer Progression via Up-Regulation of MicroRNA-195-5p

Long Non-coding RNA AGAP2-AS1 Silencing Inhibits PDLIM5 Expression Impeding Prostate Cancer Progression via Up-Regulation of MicroRNA-195-5p

The LncRNA FGD5‐AS1/miR‐497‐5p axis regulates septin 2 (SEPT2) to accelerate cancer progression and increase cisplatin‐resistance in laryngeal squamous cell carcinoma

Knockdown of Long Non-coding RNA LINC00473 Protects CHON-001 Cells against Interleukin-1β-Induced Cell Injury

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