&lt;p&gt;Neuropilin-1 Interacts with Fibronectin-1 to Promote Epithelial–Mesenchymal Transition Progress in Gastric Cancer&lt;/p&gt;

Wu, Chao; Zeng, Menghua; Liao, Gang; Qian, Kun; Li, Hui

doi:10.2147/ott.s275327

Cited by 21 publications

(15 citation statements)

References 28 publications

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“…FN1 was found overexpressed in some cancers, such as esophageal cancer and cervical cancer 34,35 . FN1 overexpression promotes gastric cancer cell migration and invasion 36 . Suppression of FN1 hampers malignant progression of colorectal carcinogenesis by inhibiting cell proliferation, migration 37 .…”

Section: Discussionmentioning

confidence: 99%

LINC02381 aggravates breast cancer through the miR‐1271‐5p/FN1 axis to activate PI3K/AKT pathway

Huang

Wang

et al. 2021

Molecular Carcinogenesis

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Emerging investigations have demonstrated that lncRNAs are key crucial modulators in cancer. In this study, we investigated the role of LINC02381 in breast cancer (BC). Reverse transcriptase quantitative polymerase chain reaction measured the LINC02381 level in BC tissues and cells. Colony formation, EdU staining, wound healing and Transwell experiments examined the impact of LINC02381 depletion on BC cell phenotypes. Relationship among miR‐1271‐5p, LINC02381, and FN1 was tested through applying RIP, luciferase reporter, and RNA pull‐down assays. We found that LINC02381 expression was elevated in BC. Functionally, LINC02381 knockdown hampered BC cell proliferation, migration, and invasion. LINC02381 overexpression accelerated tumor formation in vivo. Mechanistically, LINC02381 acted as a ceRNA to increase FN1 via decoying miR‐1271‐5p. Additionally, LINC02381 activated PI3K/AKT pathway by upregulating FN1. Rescue assays indicated that FN1 upregulation or PI3K/AKT activation rescued the LINC02381 knockdown‐mediated inhibition on malignant phenotypes of BC cells. Overall, LINC02381 exerts carcinogenic effects in BC by the miR‐1271‐5p/FN1 axis to activate PI3K/AKT pathway.

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Section: Discussionmentioning

confidence: 99%

LINC02381 aggravates breast cancer through the miR‐1271‐5p/FN1 axis to activate PI3K/AKT pathway

Huang

Wang

et al. 2021

Molecular Carcinogenesis

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“…Assessing EMT state in tumors is challenging as the process is transient and reversible (24). Previous studies have focused on exploring the biological functions and molecular mechanisms of EMT-related genes, such as the expression of E-cadherin, claudins, ocludins, and cytokeratins, and considered these genes as common markers of epithelial state, and Vimentin (VIM), fibronectin, and a-SMA as the markers of mesenchymal state (25)(26)(27). However, for some circulating tumor cells (CTCs) underwent EMT, the expression of these (25-27) epithelial cell adhesion-based molecular markers is difficult to be detected (28).…”

Section: Discussionmentioning

confidence: 99%

Identification of a Three-Gene Signature Based on Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Through Construction and Validation of a Risk-Prediction Model

et al. 2021

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Epithelial-mesenchymal transition (EMT) process, which is regulated by genes of inducible factors and transcription factor family of signaling pathways, transforms epithelial cells into mesenchymal cells and is involved in tumor invasion and progression and increases tumor tolerance to clinical interventions. This study constructed a multigene marker for lung predicting the prognosis of lung adenocarcinoma (LUAD) patients by bioinformatic analysis based on EMT-related genes. Gene sets associated with EMT were downloaded from the EMT-gene database, and RNA-seq of LUAD and clinical information of patients were downloaded from the TCGA database. Differentially expressed genes were screened by difference analysis. Survival analysis was performed to identify genes associated with LUAD prognosis, and overlapping genes were taken for all the three. Prognosis-related genes were further determined by combining LASSO regression analysis for establishing a prediction signature, and the risk score equation for the prognostic model was established using multifactorial COX regression analysis to construct a survival prognostic model. The model accuracy was evaluated using subject working characteristic curves. According to the median value of risk score, samples were divided into a high-risk group and low-risk group to observe the correlation with the clinicopathological characteristics of patients. Combined with the results of one-way COX regression analysis, HGF, PTX3, and S100P were considered as independent predictors of LUAD prognosis. In lung cancer tissues, HGF and PTX3 expression was downregulated and S100P expression was upregulated. Kaplan-Meier, COX regression analysis showed that HGF, PTX3, and S100P were prognostic independent predictors of LUAD, and high expressions of all the three were all significantly associated with immune cell infiltration. The present study provided potential prognostic predictive biological markers for LUAD patients, and confirmed EMT as a key mechanism in LUAD progression.

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“…Growing evidence has demonstrated that NRP-1 was frequently overexpressed and associated with poor prognosis in gastric cancer, melanoma, bladder cancer, cervical cancer, hepatocellular carcinoma, as well as breast cancer [ 28 - 33 ]. Our previous studies demonstrated that NRP-1 acts as an oncogene in breast cancer progression [ 5 - 8 ].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA RP11-70C1.3 confers chemoresistance of breast cancer cells through miR-6736-3p/NRP-1 axis

Zhang

Zheng

Shen

et al. 2021

Bosn J of Basic Med Sci

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Chemoresistance remains a major obstacle for improving the clinical outcome of patients with breast cancer. Recently, long noncoding RNAs (lncRNAs) have been implicated in breast cancer chemoresistance. However, the function and underlying mechanism are still largely unknown. Using lncRNA microarray, we identified 122 upregulated and 475 downregulated lncRNAs that might be related to the breast cancer chemoresistance. Among them, RP11-70C1.3 was one of the most highly expressed lncRNAs. In breast cancer patients, high RP11-70C1.3 expression predicted poor prognosis. Knockdown of RP11-70C1.3 inhibited the multidrug resistance of breast cancer cells in vitro and in vivo. Further investigations revealed that RP11-70C1.3 functioned as a competing endogenous RNA (ceRNA) for miR-6736-3p to increase NRP-1 expression. Notably, the rescue experiments showed that both miR-6736-3p inhibitor and NRP-1 overexpression could partly reverse the suppressive influence of RP11-70C1.3 knockdown on breast cancer chemoresistance. In conclusion, our study indicated that lncRNA RP11-70C1.3 regulated NRP-1 expression by sponging miR-6736-3p to confer chemoresistance of breast cancer cells. RP11-70C1.3 might be a potential therapeutic target in enhancing the clinical efficacy of chemotherapy in breast cancer.

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<p>Neuropilin-1 Interacts with Fibronectin-1 to Promote Epithelial–Mesenchymal Transition Progress in Gastric Cancer</p>

Cited by 21 publications

References 28 publications

LINC02381 aggravates breast cancer through the miR‐1271‐5p/FN1 axis to activate PI3K/AKT pathway

LINC02381 aggravates breast cancer through the miR‐1271‐5p/FN1 axis to activate PI3K/AKT pathway

Identification of a Three-Gene Signature Based on Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Through Construction and Validation of a Risk-Prediction Model

Long noncoding RNA RP11-70C1.3 confers chemoresistance of breast cancer cells through miR-6736-3p/NRP-1 axis

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