RETRACTED ARTICLE: The fibrotic microenvironment promotes the metastatic seeding of tumor cells into the lungs via mediating the ZEB1-AS1/miR-200b-3p/ZEB1 signaling

Liu, Jingjing; Meng, Jian; Li, Yuanyuan; Deng, Pengbo; Pan, Pinhua; Yang, Huanming

doi:10.1080/15384101.2020.1826236

Cited by 7 publications

(5 citation statements)

References 44 publications

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“…In our summary, lncRNA XIST is the most mentioned ceRNA-based regulation of miR-200b-3p, and it can induce HCC as well as CRC progression by inhibiting miR-200b-3p (7,10,11). ZEB1-AS1 can also act as a ceRNA to inhibit miR-200b-3p as reported by Liu et al (50), with similar inhibitory effects on the miRNA observed in other cancers. For instance, H19 participates in the metastasis of HCC by reducing miR-200b-3p levels (12).…”

Section: Mechanism Of Mir-200b-3p Regulationsupporting

confidence: 78%

“…For HCC, microRNAs can display tumor-suppressive effects, with its most important mechanism of action being the inhibition of epithelial-mesenchymal transition (EMT) by acting on ZEB1/2. Indeed, ZEB1, as an important regulator in tumors (47), promotes EMT by downregulating or upregulating E-cadherin (48) and vimentin (49) respectively and it has been shown that, by acting on both ZEB1 and ZEB2, miR-200b-3p can silence their mRNAs to downregulate their expression, thus suppressing EMT as well as reducing metastasis in HCC (10,12,50). Interestingly, similar mechanisms have also been reported for CRC (7), pancreatic cancer (14), breast carcinoma (17), and bladder cancer (30).…”

Section: Mir-200b-3p and Its Functions In Hepatocellular Carcinomamentioning

confidence: 99%

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Regulatory functions of miR‑200b‑3p in tumor development (Review)

Chen

Yuan

et al. 2022

Oncol Rep

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MicroRNAs (miRNAs/miRs), non-coding single-stranded RNAs of length 18-24 nucleotides, can modulate gene expression through post-transcriptional control. As such, they can influence tumor proliferation, apoptosis, invasion, metastasis as well as chemotherapy resistance by regulating certain downstream genes. In this context, miR-200b-3p, one particular member of the miR-200 family, possesses the ability to suppress tumor progression. However, many studies have suggested that, in certain cases, this miRNA may also promote the development of some tumors due to differences in the microenvironments and molecular backgrounds of different cancers. This review summarizes previous studies on the involvement of miR-200b-3p in tumors, including the underlying mechanism. Contents 1. Introduction 2. Mechanism of action of miR-200b-3p in cancer 3. miR-200b-3p function is dependent on cancer type 4. Mechanism of miR-200b-3p regulation 5. Conclusion

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Section: Mechanism Of Mir-200b-3p Regulationsupporting

confidence: 78%

Section: Mir-200b-3p and Its Functions In Hepatocellular Carcinomamentioning

confidence: 99%

Regulatory functions of miR‑200b‑3p in tumor development (Review)

Chen

Yuan

et al. 2022

Oncol Rep

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“…[45][46][47][48] However, other reports have pointed out that miR-200b-3p can exert oncogenic functions as showing the promotion of tumor progression by downregulating some tumor suppressor genes, including cassette subfamily A member 1 (ABAC1), large tumor suppressor kinase 2 (LATS2) and transcriptional intermediary factor 1 γ (TIF1γ). [49][50][51] In addition, miR-200b-3p may has a different functions according to the type of tumor. Although miR-200b exhibits tumor-suppressive effects in a number of tumor type, they mainly acted as an oncogene in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of exosomal microRNA panel as diagnostic and prognostic biomarker for small cell lung cancer

Rho

Kim

Park

et al. 2023

Preprint

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Small cell lung cancer (SCLC) has an exceptionally poor prognosis; as most of the cases are initially diagnosed as extensive disease with hematogenous metastasis. Therefore, the early diagnosis of SCLC is very important and may improve its prognosis. To investigate the feasibility of early diagnosis of SCLC, we examined exosomal microRNAs (miRNAs) present in serum obtained from patients with SCLC. First, exosomes were isolated in serum from patients with SCLC and healthy individuals and were characterized using particle size and protein markers. Additionally, miRNA array was performed to define SCLC-specific exosomal miRNAs. From the miRNA array results, we selected 51-miRNAs based on p-values and top 10 differentially expressed genes, and 25-miRNAs were validated using quantitative reverse transcription-polymerase chain reaction. Second, the 25-miRNAs were further validated employing a large cohort. Among them, 7-miRNAs showed significant differences. Furthermore, 6-miRNAs (miR-3565, miR-3124-5p, miR-200b-3p, miR-6515, miR-3126-3p and miR-9-5p) were up-regulated and 1-miRNA (miR-92b-5p) was down-regulated. Finally, the ability to diagnose SCLC of the 7-miRNAs was estimated by area under the curve (AUC). The AUC value of each miRNA sets between 0.64 and 0.76, however the combined application of 3-miRNAs (miR-200b-3p, miR-3124-5p and miR-92b-5p) remarkably improved the diagnostic value (AUC=0.93). Gene ontology analysis revealed that the 3-miRNA panel is linked to various oncogene pathways and nervous system development. When the 3-miRNAs were introduced to cells, the resulting changes in total mRNA expression strongly indicated the presence of lung diseases, including lung cancer. In addition, the 3-miRNA panel was significantly associated with a poorer prognosis, although individual miRNAs have not been validated as prognostic markers. In conclusion, our study identified SCLC-specific exosomal miRNAs, and the 3-miRNAs panel (miR-200b-3p, miR-3124-5p and miR-92b-5p) may serve as a diagnostic and prognostic marker for SCLC.

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“…The study has shown that ZEB1 is a key factor in the tumor microenvironment and for maintaining tumor-associated macrophages (TAMs)’ tumor-promoting functions ( 33 ). The fibrotic microenvironment promotes the spread of tumor cells to the lungs by mediating the ZEB1-AS1/miR-200b-3p/ZEB1 signaling pathway ( 34 ). Removing ZEB1 reduces the ability of breast cancer cells to grow, spread, and change their characteristics.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid receptor regulates the epithelial-mesenchymal transition process through GR/ZEB1/E-cad and is involved in breast cancer endocrine drug resistance—a bioinformatics analysis

Tang,

Ma,

Zhang

et al. 2023

Transl Cancer Res

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Background Studies have shown that there is a connection between estrogen receptor (ER) and glucocorticoid receptor (GR), which can impact the epithelial-mesenchymal transition (EMT) process and contribute to endocrine resistance in breast cancer. However, the specific mechanism is unclear. It is crucial to investigate this mechanism further. Methods This study aimed to confirm the role of GR in breast cancer endocrine resistance. Based on our hypothesis, GR is linked to a gene involved in the EMT process, and thus contributes to endocrine resistance in breast cancer. We obtained survival data and GR expression data from Molecular Taxonomy of Breast Cancer International Consortium (METABRIC). Additionally, we gathered GR expression data from Gene Expression Omnibus (GEO). Using Cytoscape, we constructed a protein-protein interaction (PPI) network and identified key genes. Data of Vimentin, E-cad, and Wnt/β-catenin expression were obtained from The Cancer Genome Atlas (TCGA). We used the co-expression method to identify key proteins. UALCAN and cBioPortal were utilized to verify the function of the key protein. Results In ER+ breast cancer, GR (P=3.12780899271121E−08) and zinc finger E-box binding homeobox 1 (ZEB1) (P=1.716157E−01) were lowly expressed and down-regulated genes of GR differentially expressed genes were enriched in cell adhesion molecules. We screened for the key protein ZEB1 and found high levels of it was positively associated with prolonged recurrence-free survival (RFS) in patients receiving endocrine therapy (P=0.0024), while high levels of E-cad were negatively associated (P=0.0038). GR expression was positively associated with ZEB1 (Spearman =0.29, P=8.50e−21), negatively associated with E-cad (Spearman =−0.13, P=5.17e−5), and negatively associated with the SETD1B (Spearman =−0.14, P=1.527e−5), a gene downstream of ZEB1. In contrast, ZEB1 expression was negatively correlated with E-cad (Spearman =−0.081, P=3.132e−3) and negatively correlated with SET domain-containing 1B (SETD1B) (Spearman =−0.177, P=9.07e−11). Conclusions In ER+ breast cancers, GR expression is suppressed, and the EMT process is inhibited by suppressing ZEB1 expression and thus promoting E-cad expression. For the investigation of endocrine medication resistance in breast cancer, it is crucial to identify the mechanisms by how GR participates in the EMT process.

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RETRACTED ARTICLE: The fibrotic microenvironment promotes the metastatic seeding of tumor cells into the lungs via mediating the ZEB1-AS1/miR-200b-3p/ZEB1 signaling

Cited by 7 publications

References 44 publications

Regulatory functions of miR‑200b‑3p in tumor development (Review)

Regulatory functions of miR‑200b‑3p in tumor development (Review)

Identification of exosomal microRNA panel as diagnostic and prognostic biomarker for small cell lung cancer

Glucocorticoid receptor regulates the epithelial-mesenchymal transition process through GR/ZEB1/E-cad and is involved in breast cancer endocrine drug resistance—a bioinformatics analysis

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