Searching the Resource Information Network

Our searching services are busy right now. Please try again later

  • Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

Roles of the H19/microRNA‑675 axis in the proliferation and epithelial‑mesenchymal transition of human cutaneous squamous cell carcinoma cells.

Wenqing Zhang | Kaili Zhou | Xue Zhang | Chenglong Wu | Dan Deng | Zhirong Yao
Oncology reports | 2021

The long non‑coding RNA (lncRNA) H19 and microRNA(miR)‑675 were reported to serve an important role in the tumorigenesis and metastasis of numerous cancer types by promoting the epithelial‑mesenchymal transition (EMT) process; however, the underlying mechanisms of action of H19 and miR‑675 in cutaneous squamous cell carcinoma (cSCC) remain unknown. The mRNA expression levels of H19 and miR‑675 were analyzed using reverse transcription‑quantitative PCR, and Cell Counting Kit‑8, wound healing and Transwell assays were performed to analyze the cell proliferation, migration and invasion of cSCC cells, respectively. The levels of cell apoptosis were also determined using a TUNEL assay. Protein expression levels of p53 and marker proteins related to the EMT process were analyzed using western blotting. In addition, a dual luciferase reporter assay was performed to determine the interactions between H19, miR‑675 and p53. The results of the present study revealed that the expression levels of H19 and miR‑675 were upregulated in cSCC tissues and cSCC cell lines. The knockdown of H19 or miR‑675 expression inhibited cell proliferation, migration and invasion, but induced cell apoptosis. In addition, the expression levels of EMT‑related markers were also downregulated. The overexpression of H19 upregulated the expression levels of its predicted target, miR‑675, which subsequently promoted the EMT process and downregulated the expression levels of p53. Conversely, the genetic silencing of H19 or miR‑675 inhibited proliferation and invasion in SCL1 and A431 cSCC cell lines. In conclusion, the findings of the present study provided novel insight into the potential role of H19 and miR‑675 in the development, metastasis and progression of cSCC, which may help the development of treatments for cSCC.

Pubmed ID: 33649811

Research resources used in this publication

None found

Antibodies used in this publication

None found

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.


Cell Signaling Technology (tool)

RRID:SCR_004431

Privately held company that develops and produces antibodies, ELISA kits, ChIP kits, proteomic kits, and other related reagents used to study cell signaling pathways that impact human health.

View all literature mentions

Bio-Rad Laboratories (tool)

RRID:SCR_008426

Commercial instrument and chemical vendor. Developer and manufacturer of specialized technological products for life science research and clinical diagnostics markets.

View all literature mentions

Thermo Fisher Scientific (tool)

RRID:SCR_008452

Commercial vendor and service provider of laboratory reagents and antibodies. Supplier of scientific instrumentation, reagents and consumables, and software services.

View all literature mentions

Millipore (tool)

RRID:SCR_008983

An Antibody supplier

View all literature mentions

Abcam (tool)

RRID:SCR_012931

A commercial antibody supplier which supplies primary and secondary antibodies, biochemicals, proteins, peptides, lysates, immunoassays and other kits.

View all literature mentions

HaCaT (tool)

RRID:CVCL_0038

Cell line HaCaT is a Spontaneously immortalized cell line with a species of origin Homo sapiens (Human)

View all literature mentions