Accumulating evidence has established that long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) is a tumor regulator in many cancers. Here, we aimed to investigate the possible ...function of lncRNA PVT1 in esophageal carcinoma (EC) via targeting of microRNA‐145 (miR‐145). Initially, microarray‐based gene expression profiling of EC was employed to identify differentially expressed genes. Moreover, the expression of lncRNA PVT1 was examined and the cell line presenting with the highest level of lncRNA PVT1 expression was selected for subsequent experiments. We then proceeded to examine interaction among lncRNA PVT1, FSCN1, and miR‐145. The effect of lncRNA PVT1 on viability, migration, invasion, apoptosis, and tumorigenesis of transfected cells was examined with gain‐of‐function and loss‐of‐function experiments. We observed that lncRNA PVT1 was robustly induced in EC. lncRNA PVT1 could bind to miR‐145 and regulate its expression, and FSCN1 is a target gene of miR‐145. Overexpression of miR‐145 or silencing of lncRNA PVT1 was revealed to suppress cell viability, migration, and invasion abilities, while also stimulating cell apoptosis. Furthermore, our in vivo results showed that overexpression of miR‐145 or silencing of lncRNA PVT1 resulted in decreased tumor growth in nude mice. In conclusion, our research reveals that down‐regulation of lncRNA PVT1 could potentially promote expression of miR‐145 to repress cell migration and invasion, and promote cell apoptosis through the inhibition of FSCN1. This highlights the potential of lncRNA PVT1 as a therapeutic target for EC treatment.
lncRNA PVT1 can specifically compete with miR‐145 to inhibit its expression, thereby increasing FSCN1 expression. This in turn promotes proliferation, invasion, and migration of EC cells by up‐regulating the expression of MAT1, CD147, and VEGFR2. Moreover, down‐regulation of lncRNA PVT1 can up‐regulate expression of miR‐145 to inhibit the expression of FSCN1.
Objective To investigate the effect of lncRNA HEIH on proliferation and apoptosis of lung cancer cells and its mechanism. Methods Human lung epithelial cells BEAS-2B and lung cancer cell lines A549, ...A427, H1299 and TKB-1 were cultured, and the expression level of HEIH was detected by RT-qPCR. Si-HEIH and miR-98-5p mimics were transfected into A549 cells inorder to silence the expression of HEIH in A549 cells or over-expressing miR-98-5p. Then cell proliferation was detected by MTT assay, apoptosis was examined by flow cytometry, and the levels of CCND1, caspase-3, SHH, GLI-1, PTCH and SUFU proteins were measured by Western blot. The dual luciferase reporter gene assay verified the relationship between HEIH and miR-98-5p. Results Compared with the normal lung epithelial cells BEAS-2B, the levels of HEIH in lung cancer cell lines,A549, A427, H1299 and TKB-1 were significantly increased (P＜0.05). Among them,the level of HEIH in lung cancer celllines A549 was the highest. Therefore, A549 cells were selected as th
It is still controversial whether patients with clinical T2N0M0 (cT2N0M0) esophageal cancer are treated with induction therapy. The aim of this study was to determine the effect of induction therapy ...on cT2N0M0 esophageal cancer.
We searched PubMed, Embase, the Cochrane Library, and Medline databases from inception up to May 1, 2017. This meta-analysis was performed to compare odds ratios (OR) for 5-year overall survival (OS), pathologically understaged and overstaged after esophagectomy.
Eight retrospective studies of 2646 patients were included in the meta-analysis. Data showed that no statistically significant difference in 5-year over survival was observed between induction therapy group and direct operation group. The pooled OR and 95% confidence interval (CI) for 5-year OS were 0.92 (95% CI = 0.72-1.18; P = .52). Whereas, compared with induction therapy group, direct operation group had more pathologically understaged and less overstaged after esophagectomy.
Currentclinical staging for T2N0M0 esophageal carcinoma remains inaccurate. In this study, we found that direct operation group had more pathologically understaged and less overstaged after esophagectomy compared with induction therapy group. Induction therapy could degrade the tumor staging but not improve the patient's survival.
Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) is correlated to various malignant tumors. Consequently, we explored effects of lncRNA PVT1 on esophageal carcinoma (EC) ...targeting microRNA-145 (miR-145). EC tissues, adjacent normal tissues, and EC-related cell lines were collected and cultured. Expression of lncRNA PVT1, miR-145, fascin-1 (FSCN1), and related genes with intervening expression of PVT1 and miR-145 was determined. Bioinformatic website, dual-luciferase reporter assay, and RNA immunoprecipitation (RIP) were carried to verify target relationship among lncRNA PVT1, FSCN1, and miR-145. Scratch test, Transwell assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and flow cytometry were performed for detection of migration, invasion, viability, and apoptosis of transfected cells, respectively. Finally, tumor formation in nude mice was measured. After database analysis, lncRNA PVT1, miR-145, and FSCN1 were selected for study. lncRNA PVT1 and FSCN1 can bind to miR-145. After overexpressing miR-145 or inhibiting lncRNA PVT1, EC cell viability, migration, and invasion were inhibited, while volume and weight of tumor formation in nude mice decreased. Expression of lncRNA PVT1, FSCN1, Bcl-2, CD147, VEGFR2, and MTA1 decreased and expression of miR-145 and Bax increased. Silencing lncRNA PVT1 can upregulate miR-145, which is a tumor suppressor in EC via knockdown of FSCN1. Thus, we might provide a potential theoretical basis for EC treatment.
Accumulating evidence has established that long noncoding
RNA
(lnc
RNA
) plasmacytoma variant translocation 1 (
PVT
1) is a tumor regulator in many cancers. Here, we aimed to investigate the possible ...function of lnc
RNA PVT
1 in esophageal carcinoma (
EC
) via targeting of micro
RNA
‐145 (miR‐145). Initially, microarray‐based gene expression profiling of
EC
was employed to identify differentially expressed genes. Moreover, the expression of lnc
RNA PVT
1 was examined and the cell line presenting with the highest level of lnc
RNA PVT
1 expression was selected for subsequent experiments. We then proceeded to examine interaction among lnc
RNA PVT
1,
FSCN
1, and miR‐145. The effect of lnc
RNA PVT
1 on viability, migration, invasion, apoptosis, and tumorigenesis of transfected cells was examined with gain‐of‐function and loss‐of‐function experiments. We observed that lnc
RNA PVT
1 was robustly induced in
EC
. lnc
RNA PVT
1 could bind to miR‐145 and regulate its expression, and
FSCN
1 is a target gene of miR‐145. Overexpression of miR‐145 or silencing of lnc
RNA PVT
1 was revealed to suppress cell viability, migration, and invasion abilities, while also stimulating cell apoptosis. Furthermore, our
in vivo
results showed that overexpression of miR‐145 or silencing of lnc
RNA PVT
1 resulted in decreased tumor growth in nude mice. In conclusion, our research reveals that down‐regulation of lnc
RNA PVT
1 could potentially promote expression of miR‐145 to repress cell migration and invasion, and promote cell apoptosis through the inhibition of
FSCN
1. This highlights the potential of lnc
RNA PVT
1 as a therapeutic target for
EC
treatment.
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).
This article has been retracted at the request of the Authors.
The ...article is a duplicate of a paper that has already been published: Shen et al., 2019, Mol. Oncol., 13, 2554–2573, https://doi.org/10.1002/1878-0261.12555.
Redundant publications overweigh the relative importance of published findings and distort the academic record of the authors. One of the conditions of submission of a paper for publication is therefore that authors declare explicitly that the paper has not been previously published and is not under consideration for publication elsewhere. As such, this article represents a misuse of the scientific publishing system.
The scientific community takes a very strong view on this matter, and apologies are offered to readers of the journal that this was not detected during the submission process.
Accumulating evidence has established that long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) is a tumor regulator in many cancers. Here, we aimed to investigate the possible ...function of lncRNA PVT1 in esophageal carcinoma (EC) via targeting of microRNA‐145 (miR‐145). Initially, microarray‐based gene expression profiling of EC was employed to identify differentially expressed genes. Moreover, the expression of lncRNA PVT1 was examined and the cell line presenting with the highest level of lncRNA PVT1 expression was selected for subsequent experiments. We then proceeded to examine interaction among lncRNA PVT1, FSCN1, and miR‐145. The effect of lncRNA PVT1 on viability, migration, invasion, apoptosis, and tumorigenesis of transfected cells was examined with gain‐of‐function and loss‐of‐function experiments. We observed that lncRNA PVT1 was robustly induced in EC. lncRNA PVT1 could bind to miR‐145 and regulate its expression, and FSCN1 is a target gene of miR‐145. Overexpression of miR‐145 or silencing of lncRNA PVT1 was revealed to suppress cell viability, migration, and invasion abilities, while also stimulating cell apoptosis. Furthermore, our in vivo results showed that overexpression of miR‐145 or silencing of lncRNA PVT1 resulted in decreased tumor growth in nude mice. In conclusion, our research reveals that down‐regulation of lncRNA PVT1 could potentially promote expression of miR‐145 to repress cell migration and invasion, and promote cell apoptosis through the inhibition of FSCN1. This highlights the potential of lncRNA PVT1 as a therapeutic target for EC treatment.
Purpose:
Graft-versus-host disease (GVHD) is an important complication after human leukocyte antigen (HLA) haploidentical donor (HID) hematopoietic stem cell transplantation (HSCT), which may lead to ...poor prognosis. Our study intends to identify the efficacy and safety of mesenchymal stem cells (MSCs) for multidrug-resistant (MDR)-GVHD after HID HSCT.
Methods:
MDR-GVHD was referring to GVHD remaining no response to at least two types of therapy, and hUCB-MSCs were given at the dose of (1.0–2.0) × 106/kg once a week.
Results:
A total of 21 patients were enrolled in this retrospective study (acute GVHD (aGVHD): n = 14, chronic GVHD (cGVHD): n = 7). The median dose of MSCs was 1.2 × 106 cells/kg (range, 0.8–1.8 × 106) cells/kg, and the median numbers of infusion were 2 (range, 1–7) and 3 (range, 2–12) for MDR-aGVHD and MDR-cGVHD patients, respectively. In MDR-aGVHD patients, the overall response rate (ORR) was 57.1%, including 50.0% complete response (CR) and 7.1% partial response (PR), and the median time to response was 49.5 days (range, 16–118) days. The 2-year probability of overall survival after MSCs was 64.3%. Five patients (35.7%) developed infections after MSCs, and no obvious hematologic toxicities were observed. Five MDR-aGVHD patients died after MSCs treatments because of GVHD progression (n = 1), severe infection (bacterial central nervous system infection: n = 1; fungal pneumonia: n = 2), and poor graft function (n = 1). In MDR-cGVHD patients, three patients (42.9%) achieved PR after MSCs and the median time to response was 56 days (22–84) days. The ORRs for moderate and severe cGVHD were 50.0% and 33.3%, respectively. Four MDR-cGVHD patients died after MSCs treatments because of GVHD progression (n = 2), severe fungal pneumonia (n = 1), and relapse (n = 1).
Conclusion:
MSCs treatment may be safe and effective for MDR-GVHD after HID HSCT.
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