SP1-induced overexpression of LINC00520 facilitates non-small cell lung cancer progression through miR-577/CCNE2 pathway and predicts poor prognosis

Wang, Jifang; Xi, Zhuona; Su, Hongjian; Bao, Zhen; Qiao, Yahong

doi:10.1007/s13577-021-00518-y

Cited by 15 publications

(22 citation statements)

References 33 publications

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“…An increasing number of studies have revealed that Sp1 regulates the expression of many noncoding genes. Recent studies have indicated that Sp1-induced overexpression of LINC00520 facilitates NSCLC progression through the miR-577/CCNE2 pathway and predicts poor prognosis [ 47 ]. Sp1-induced AFAP1-AS1 contributes to proliferation and invasion by regulating the miR-497-5p/CELF1 pathway in nasopharyngeal carcinoma [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Estradiol-mediated inhibition of Sp1 decreases miR-3194-5p expression to enhance CD44 expression during lung cancer progression

et al. 2022

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Background Sp1, an important transcription factor, is involved in the progression of various cancers. Our previous studies have indicated that Sp1 levels are increased in the early stage of lung cancer progression but decrease during the late stage, leading to poor prognosis. In addition, estrogen has been shown to be involved in lung cancer progression. According to previous studies, Sp1 can interact with the estrogen receptor (ER) to coregulate gene expression. The role of interaction between Sp1 and ER in lung cancer progression is still unknown and will be clarified in this study. Methods The clinical relevance between Sp1 levels and survival rates in young women with lung cancer was studied by immunohistochemistry. We validated the sex dependence of lung cancer progression in EGFRL858R-induced lung cancer mice. Wound healing assays, chamber assays and sphere formation assays in A549 cells, Taxol-induced drug-resistant A549 (A549-T24) and estradiol (E2)-treated A549 (E2-A549) cells were performed to investigate the roles of Taxol and E2 in lung cancer progression. Luciferase reporter assays, immunoblot and q-PCR were performed to evaluate the interaction between Sp1, microRNAs and CD44. Tail vein-injected xenograft experiments were performed to study lung metastasis. Samples obtained from lung cancer patients were used to study the mRNA level of CD44 by q-PCR and the protein levels of Sp1 and CD44 by immunoblot and immunohistochemistry. Results In this study, we found that Sp1 expression was decreased in premenopausal women with late-stage lung cancer, resulting in a poor prognosis. Tumor formation was more substantial in female EGFRL858R mice than in male mice and ovariectomized female mice, indicating that E2 might be involved in the poor prognosis of lung cancer. We herein report that Sp1 negatively regulates metastasis and cancer stemness in E2-A549 and A549-T24 cells. Furthermore, E2 increases the mRNA and protein levels of RING finger protein 4 (RNF4), which is the E3-ligase of Sp1, and thereby decreases Sp1 levels by promoting Sp1 degradation. Sp1 can be recruited to the promoter of miR-3194-5p, and positively regulate its expression. Furthermore, there was a strong inverse correlation between Sp1 and CD44 levels in clinical lung cancer specimens. Sp1 inhibited CD44 expression by increasing the expression of miR-3194-5p, miR-218-5p, miR-193-5p, miR-182-5p and miR-135-5p, ultimately resulting in lung cancer malignancy. Conclusion Premenopausal women with lung cancer and decreased Sp1 levels have a poor prognosis. E2 increases RNF4 expression to repress Sp1 levels in premenopausal women with lung cancer, thus decreasing the expression of several miRNAs that can target CD44 and ultimately leading to cancer malignancy.

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Section: Discussionmentioning

confidence: 99%

Estradiol-mediated inhibition of Sp1 decreases miR-3194-5p expression to enhance CD44 expression during lung cancer progression

et al. 2022

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“…LINC00520 is abnormally upregulated in 11 cancers, including lung cancer ( 11 ), non-small cell lung cancer (NSCLC) ( 10 ), lung adenocarcinoma (LUAD) ( 12 , 13 ), breast cancer (BC) ( 4 , 8 ), papillary thyroid carcinoma (PTC) ( 14 ), colorectal cancer (CRC) ( 15 ), melanoma (MM) ( 16 – 18 ), head and neck squamous cell carcinoma (HNSCC) ( 19 ), laryngeal squamous cell carcinoma (LSCC) ( 20 ), glioma ( 9 ), nasopharyngeal carcinoma (NPC) ( 21 ), etc. Further in vitro experiments have shown that LINC00520 significantly promotes tumor progression by controlling the proliferation and other biological functions of cancer cells ( 14 , 21 ) ( Table 1 ).…”

Section: The Aberrant Expression Of Linc00520 In Cancermentioning

confidence: 99%

“…As shown in Table 2 , LINC00520 can predict a poor prognosis for a variety of cancers. Generally, cancer patients with lower LINC00520 expression levels have a higher overall survival rate (OS), including lung cancer ( 11 ), LUAD ( 13 ), NSCLC ( 10 ), PTC ( 14 ), CRC ( 15 ), MM ( 16 , 18 ), and NPC ( 21 ).…”

Section: The Association Of Linc00520 Expression With the Prognostic ...mentioning

confidence: 99%

“…In lung cancer, the level of LINC00520 in patients with stage III+IV is higher than that of patients with stage I+II ( 11 ). In NSCLC, high LINC00520 levels are significantly associated with advanced tumor stage and positive lymph node metastasis ( 10 ). In PTC, the high expression of LINC00520 is significantly related to increased tumor size, lymph node metastasis, and advanced TNM stage of PTC patients ( 14 ).…”

Section: The Association Of Linc00520 Expression With the Prognostic ...mentioning

confidence: 99%

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LINC00520: A Potential Diagnostic and Prognostic Biomarker in Cancer

Zhang

Shen

et al. 2022

Front. Immunol.

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Long non-coding RNA (lncRNA) is important in the study of cancer mechanisms. LINC00520 is located on human chromosome 14q22.3 and is a highly conserved long non-coding RNA. LINC00520 is widely expressed in various tissues. The expression of LINC00520 is regulated by transcription factors such as Sp1, TFAP4, and STAT3. The high expression of LINC00520 is significantly related to the risk of 11 cancers. LINC00520 can competitively bind 10 miRNAs to promote tumor cell proliferation, invasion, and migration. In addition, LINC00520 is involved in the regulation of P13K/AKT and JAK/STAT signaling pathways. The expression of LINC00520 is significantly related to the clinicopathological characteristics and prognosis of tumor patients and is also related to the sensitivity of HNSCC to radiotherapy. Here, this article summarizes the abnormal expression pattern of LINC00520 in cancer and its potential molecular regulation mechanism and points out that LINC00520 can be used as a potential biomarker for cancer diagnosis, prognosis, and treatment.

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“…MicroRNA-577 (miR-577) and microRNA-1224-5p (miR-1224-5p) are microRNAs, which have been proved to participate in the progression of various cancers. For example, miR-577 suppressed progression of multiple cancers, such as non-small cell lung cancer [ 15 ], liver cancer [ 16 ] and gastric cancer [ 17 ]. In addition, miR-1224-5p has been determined as an inhibitor in malignant development of rectal cancer [ 18 ] and esophageal squamous cell carcinoma [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA nuclear-enriched abundant transcript 1 (LncRNA NEAT1) upregulates Cyclin T2 (CCNT2) in laryngeal papilloma through sponging miR-577/miR-1224-5p and blocking cell apoptosis

Zhao

Hou

2022

Bioengineered

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Long non-coding RNA nuclear-enriched abundant transcript 1 (Lnc-NEAT1) is a crucial mediator in cancer progression, which is associated with poor prognosis of patients with laryngeal papilloma (LP). Herein, we aimed to determine how Lnc-NEAT1 promotes LP development. q-PCR, MTT, EDU and Western blotting were performed to determine that Lnc-NEAT1 facilitates LP cell proliferation and hinders cell apoptosis. LncBase database, q-PCR, GEPIA online database, Dual luciferase reporter and RIP assays were utilized to confirm that Lnc-NEAT1 sponged miR-577/miR-1224-5p and negatively mediated CCNT2. Western blotting, MTT and EDU were used to confirm that Lnc-NEAT1 promoted LP cell proliferation and inhibited cell apoptosis through CCNT2. Lnc-NEAT1 was highly expressed in LP, and enhanced LP cell proliferation, and it was inhibited by Lnc-NEAT1 depleting. Concerning the underlying mechanism, it was found that Lnc-NEAT1 could functionally sponge microRNA-577 (miR-577) and microRNA-1224-5p (miR-1224-5p) and up-regulate Cyclin T2 (CCNT2) in LP cells. Notably, CCNT2 knockdown blocked Lnc-NEAT1-induced LP cell proliferation, and rescued cell apoptosis, which was specifically indicated by restoration of Bax, Cleaved caspase 3 and Cleaved caspase 9. Lnc-NEAT1 played a carcinogenic role in LP through mediating miR-577 or miR-1224-5p/CCNT2 axis, which may provide promising insights for the treatment of LP.

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SP1-induced overexpression of LINC00520 facilitates non-small cell lung cancer progression through miR-577/CCNE2 pathway and predicts poor prognosis

Cited by 15 publications

References 33 publications

Estradiol-mediated inhibition of Sp1 decreases miR-3194-5p expression to enhance CD44 expression during lung cancer progression

Estradiol-mediated inhibition of Sp1 decreases miR-3194-5p expression to enhance CD44 expression during lung cancer progression

LINC00520: A Potential Diagnostic and Prognostic Biomarker in Cancer

Long non-coding RNA nuclear-enriched abundant transcript 1 (LncRNA NEAT1) upregulates Cyclin T2 (CCNT2) in laryngeal papilloma through sponging miR-577/miR-1224-5p and blocking cell apoptosis

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