MiR-552-3p facilitated cell proliferation, migration and invasion by sponging Fibulin 5 in non-small cell lung cancer via activation of ERK/GSK3β/β-catenin signaling pathway

Huang, Mingfang; Liao, Xuqiang; Li, Liang; Li, Gao; Chen, Minbiao

doi:10.1016/j.tice.2021.101672

Cited by 2 publications

(3 citation statements)

References 34 publications

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“…For instance, miR-411-5p is available to restrain PCa's occurrence and development via silencing SMAD3 and TGFBR2 proteins [12]. Fibulin 5 and miR-552-3p can be combined to promote lung cancer (LC) cell growth [13].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA SMARCA5 Modulates Epithelial-Mesenchymal Transformation, Proliferation, and Metastasis of Nasopharyngeal Carcinoma Cells via microRNA-582-3p/Phosphatase and Tensin Homolog Axis

Wang

Ren

2023

Evidence-Based Complementary and Alternative Medicine

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The action mechanism in which circular RNA (circ) SMARCA5 targeted nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, and apoptosis via microRNA (miR)-582-3p/phosphatase and tensin homolog (PTEN) axis was explored. The examination was performed via reverse transcription-quantitative polymerase chain reaction (RT-qPCR), discovering that circSMARCA5 was elevated while miR-582-3p was silenced in NPC tissues and cells. E-cadherin and N-cadherin were detected. The results illustrated transfection with si-circSMARCA5 or miR-582-3p-mimic was available to repress cancer cell advancement, and E-cadherin was augmented. Transfection with pcDNA 3.1-circSMARCA5 or miR-582-3p-inhibitor was available to accelerate cancer cell advancement, and N-cadherin was augmented. MiR-582-3p-inhibitor blocked the suppression of si-circSMARCA5 on NPC. The si-PTEN blocked the malignant behavior of pcDNA 3.1-circSMARCA5 against NPC. The binding sites between circSMARCA5 and miR-582-3p and between miR-582-3p and PTEN were verified. Linear analysis results illuminated the expression pattern of circSMARCA5 was opposite to miR-582-3p, while the expression pattern of circSMARCA5 was positively associated with PTEN. In brief, the results of the research clarified circSMARCA5 modulated NPC cells’ vital movement via the miR-582-3p/PTEN molecular axis.

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Section: Introductionmentioning

confidence: 99%

Circular RNA SMARCA5 Modulates Epithelial-Mesenchymal Transformation, Proliferation, and Metastasis of Nasopharyngeal Carcinoma Cells via microRNA-582-3p/Phosphatase and Tensin Homolog Axis

Wang

Ren

2023

Evidence-Based Complementary and Alternative Medicine

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“…FBLN5 overexpression reduces tumor angiogenesis, suppresses lung adenocarcinoma and ovarian cancer progression, and has anti-tumor function [ 21 , 33 , 34 ]. In addition, FBLN5 acted as a target gene that can be regulated by miRNAs, such as miR-552/370/27a-3pp, thereby exerting the function of an anti-oncogene in NSCLC, breast cancer, and ovarian carcinoma [ 22 , 35 , 36 ]. Here, FBLN5 was found to be underexpressed in thyroid cancer, and its expression was enhanced by LINC00987 overexpression.…”

Section: Discussionmentioning

confidence: 99%

“…Fibulin-5 (FBLN5), a fibrin, has been shown to enhance endothelial cell adhesion [ 19 ]. FBLN5 reduced the invasion, mammospheres formation, and proliferation capacity of cancer cells via silencing β-catenin phosphorylation in breast cancer and NSCLC, acting as a cancer suppressor gene [ 20 – 22 ]. Whether FBLN5 acts downstream of LINC01089 regulation in thyroid cancer is unclear.…”

Section: Introductionmentioning

confidence: 99%

LINC01089 blocks malignant progression of thyroid cancer by binding miR-27b-3p to enhance the FBLN5 protein level

et al. 2022

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LINC01089 suppresses the malignant progression of breast, colorectal, and non-small cell lung cancers. However, the function of LINC01089 in thyroid cancer has not yet been elucidated. Here, The Cancer Genome Atlas (TCGA) database showed that LINC01089 expression is remarkably reduced in thyroid cancer tissues. Lower LINC01089 expression was correlated with higher tumor stage and regional lymph node metastasis. Furthermore, LINC01089 overexpression effectively blocked thyroid cancer cell proliferation, migration, and invasion. LINC01089 acted as a competing endogenous RNA for miR-27b-3p, thus inhibiting miR-27b-3p expression. miR-27b-3p overexpression promoted the proliferation, migration, and invasion of thyroid cancer, reversing the effect of LINC01089 overexpression on thyroid cancer. Fibulin-5 (FBLN5) was discovered as a target of miR-27b-3p in thyroid cancer. FBLN5 expression was found to be underexpressed in thyroid cancer and was enhanced and reduced by LINC00987 overexpression and miR-27b-3p overexpression, respectively. Furthermore, FBLN5 knockdown promoted the malignant progression of thyroid cancer cells by counteracting the effect of LINC00987. In conclusion, LINC01089 plays a tumor-suppressive role by binding miR-27b-3p to increase FBLN5 expression, confirming that LINC01089 has tremendous potential to become a therapeutic target for thyroid cancer treatment.

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MiR-552-3p facilitated cell proliferation, migration and invasion by sponging Fibulin 5 in non-small cell lung cancer via activation of ERK/GSK3β/β-catenin signaling pathway

Cited by 2 publications

References 34 publications

Circular RNA SMARCA5 Modulates Epithelial-Mesenchymal Transformation, Proliferation, and Metastasis of Nasopharyngeal Carcinoma Cells via microRNA-582-3p/Phosphatase and Tensin Homolog Axis

Circular RNA SMARCA5 Modulates Epithelial-Mesenchymal Transformation, Proliferation, and Metastasis of Nasopharyngeal Carcinoma Cells via microRNA-582-3p/Phosphatase and Tensin Homolog Axis

LINC01089 blocks malignant progression of thyroid cancer by binding miR-27b-3p to enhance the FBLN5 protein level

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