miR‐330‐3p promotes lung cancer cells invasion, migration, and metastasis by directly targeting <i>hSOD2b</i>

Shen, Lianghua; Yi, Shanze; Huang, Luyuan; Li, Shuaiguang; Bai, Fang; Lei, Sijia; Breitzig, Mason; Czachor, Alexander; Sun, Han; Zheng, Qi; Wang, Feng

doi:10.1002/bab.1691

Cited by 23 publications

(13 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is a well‐accepted fact that the aberrant expression of miRNAs play significant roles in the carcinogenesis and progression of human cancers . Therefore, in‐depth understanding of the roles of miRNAs shall provide new dimension into molecular mechanism involved in the tumor formation and growth of cancer as well for the development of novel therapeutic strategies .…”

Section: Resultsmentioning

confidence: 99%

miR‐197‐5p inhibits sarcomagenesis and induces cellular senescence via repression of KIAA0101

Jain

Roy

Das

et al. 2019

Molecular Carcinogenesis

View full text Add to dashboard Cite

The abnormal expressions of microRNAs (miRNAs) are known to be associated with various pathophysiological processes that lead to the development of a plethora of diseases including cancer. Among several miRNAs studied so far, miR-197 has been reported to play a vital role either as an oncogene or tumor suppressor in different cancers. However, its role in carcinogenesis of fibrosarcoma has not yet been elucidated. Therefore, the current study investigated the role of miR-197-5p, which is significantly downregulated in HT1080 fibrosarcoma cells compared to IMR90-tert fibroblast cells. The transient overexpression of miR-197-5p causes a significant decrease in viability and proliferation of fibrosarcoma cells in both concentration-and time-dependent manners. Interestingly, we did not observe any significant changes in cell cycle pattern or apoptotic cell populations, but rather noticed cellular senescence of fibrosarcoma cells upon overexpression of miR-197-5p. Further, this miRNA suppresses the metastatic properties, such as migration, invasion, and anchorageindependent growth of fibrosarcoma possibly through targeting KIAA0101, which is a proliferating cell nuclear antigen-associated factor and overexpressed in the malignancy. In nutshell, our result revealed that miR-197-5p acts as an oncosuppressor miRNA in fibrosarcoma through target regulation of KIAA0101, which can be exploited for developing RNA-based therapeutic strategies for the cure of this malignancy.

show abstract

Section: Resultsmentioning

confidence: 99%

miR‐197‐5p inhibits sarcomagenesis and induces cellular senescence via repression of KIAA0101

Jain

Roy

Das

et al. 2019

Molecular Carcinogenesis

View full text Add to dashboard Cite

show abstract

“…It is well‐known that miRNA can affect the pathogenesis of various diseases by specifically targeting a certain mRNA . In order to further investigate the mechanisms of miR‐330‐3p on INS‐1 cells in GDM, in this study, we found that GCK was a target gene of miR‐330‐3p.…”

Section: Discussionmentioning

confidence: 99%

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Xiao

Ding

Shi³

et al. 2020

J of Obstet and Gynaecol

View full text Add to dashboard Cite

Aims: High-expressed miR-330-3p in gestational diabetes mellitus (GDM) patients was reported. However, the role and mechanism of miR-330-3p in GDM are rarely reported. In this research, we aim to investigate the effects of miR-330-3p on GDM. Methods: MiR-330-3p expression in the GDM patients' blood was determined by q-PCR. Blood glucose of blood samples was detected using blood glucose detection kits. Glucokinase (GCK) was confirmed to be a target gene of miR-330-3p by bioinformatics and luciferase analysis. Correlations between miR-330-3p with GCK and blood glucose were analyzed by Pearson correlation analysis. After INS-1 cells were treated with glucose and transfected with mimic, inhibitor or siGCK, GCK expression was detected by western blot, and q-PCR, enzyme-linked immunosorbent assays, cell counting kit-8 and Annexin-V/propidium iodide were conducted to examine the expression of insulin, cell viability and apoptosis. Results: MiR-330-3p was high-expressed in GDM patients' blood, while GCK was low-expressed. The miR-330-3p expression level positively correlated with blood glucoseand and it was highly expressed in glucosetreated INS-1 cells (11 and 22 mmol/L), while miR-330-3p expression negatively correlated with GCK expression. GCK expression was inhibited by miR-330-3p mimic and enhanced by the miR-330-3p inhibitor. MiR-330-3p mimic inhibited INS-1 cells' insulin expression, cell viability and induced apoptosis. Yet miR-330-3p inhibitor and siGCK exhibited opposite effects which miR-330-3p mimic and GCK played on INS-1 cells. In addition, siGCK reversed the effect of miR-330-3p inhibitor on INS-1 cells. Conclusion: Our findings proved that miR-330-3p targeting GCK lead to the dysfunction of INS-1 cells in GDM, and could become a therapeutic target for GDM treatment.

show abstract

“…It was reported that miR-330-3p can target the gene of program cell death 4 (PDCD4) to promote tumor [17]. MiR-330-3p is also related with metastasis and invasion of lung cancer, and glutamate receptor 3 (GRIA3) [18] and human manganese superoxide dismutase 2 (hSOD2) [19] are its two target genes. Researches found miR-330-3p is correlated with bad prognosis in breast cancer as well [20], in which miR-330-3p can target Collagen and Calcium Binding EGF Domains 1 (CCBE1) to promote cancer metastasis [21].…”

Section: Discussionmentioning

confidence: 99%

Expression profile of SYNE3 and bioinformatic analysis of its prognostic value and functions in tumors

Liao

Zhang

Yang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Spectrin repeat containing nuclear envelope family member 3 (SYNE3) encodes an important component of linker of cytoskeleton and nucleoskeleton (LINC) complex, namely nesprin-3. In tumor, invasiveness and metastasis rely on the integrity of LINC complex, while the role of SYNE3/nesprin-3 in cancer is rarely studied. Methods: Here, we explored the expression pattern, prognostic value and related mechanisms of SYNE3 through both experimental and bioinformatic methods. We first detected SYNE3 in BALB/c mice, normal human tissues and the paired tumor tissues, then used bioinformatic databases to verify our results. We further analyzed the prognostic value of SYNE3. Next, we predicted miRNA targeting SYNE3 and built a competing endogenous RNA (ceRNA) network and a transcriptional network by analyzing data from the cancer genome atlas (TCGA) database. Interacting genes of SYNE3 were predicted, and we further performed GO and KEGG enrichment analysis on these genes. Besides, the relationship of SYNE3 and immune infiltration was also investigated. Results: SYNE3 exhibited various expressions in different tissues, mainly located on nuclear and in cytoplasm sometimes. SYNE3 expression level had prognostic value in tumors, possibly by stablizing nucleus, promoting tumor cells apoptosis and altering tumor microenvironment. Additionally, we constructed a RP11-2B6.2-miR-149-5p-/LINC01094-miR-330-3p-SYNE3 ceRNA network and a SATB1-miR-149-5p-SYNE3 transcriptional network in lung squamous cell carcinoma to support the tumor-suppressing role of SYNE3. Conclusions: Our study explored novel anti-tumor functions and mechanisms of SYNE3, which might be useful for future cancer therapy.

show abstract

miR‐330‐3p promotes lung cancer cells invasion, migration, and metastasis by directly targeting hSOD2b

Cited by 23 publications

References 51 publications

miR‐197‐5p inhibits sarcomagenesis and induces cellular senescence via repression of KIAA0101

miR‐197‐5p inhibits sarcomagenesis and induces cellular senescence via repression of KIAA0101

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Expression profile of SYNE3 and bioinformatic analysis of its prognostic value and functions in tumors

Contact Info

Product

Resources

About