MicroRNA-18a regulates the metastatic properties of oral squamous cell carcinoma cells via HIF-1α expression

Kim, Shihyun; Park, Suyeon; Oh, Ji-Hyeon; Lee, Sang Shin; Lee, Yoon; Choi, Jongho

doi:10.1186/s12903-022-02425-6

Cited by 12 publications

(3 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, Ribeiro et al demonstrated that high HIF-1α expression in OSCC tumor margins is critical in the transition from primary lesions to invasive cancer [ 45 ]. We previously found that HIF-1α expression is higher in metastatic OSCC tissues than in non-metastatic OSCC tissues [ 46 ]. These findings suggested that HIF-1α may facilitate regional metastasis from precursor lesions.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3

et al. 2023

Self Cite

View full text Add to dashboard Cite

Background Oral squamous cell carcinoma (OSCC) is a highly malignant tumor that is frequently associated with lymph node metastasis, resulting in poor prognosis and survival in patients. In the tumor microenvironment, hypoxia plays an important role in regulating cellular responses such as progressive and rapid growth and metastasis. In these processes, tumor cells autonomously undergo diverse transitions and acquire functions. However, hypoxia-induced transition of OSCC and the involvement of hypoxia in OSCC metastasis remain unclear. Therefore, in this study, we aimed to elucidate the mechanism of hypoxia-induced OSCC metastasis and particularly, its impact on tight junctions (TJs). Methods The expression of hypoxia-inducible factor 1-alpha (HIF-1α) was detected in tumor tissues and adjacent normal tissues from 29 patients with OSCC using reverse transcription quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry (IHC). The migration and invasion abilities of OSCC cell lines treated with small interfering (si)RNA targeting HIF-1α or cultured in hypoxic conditions were analyzed using Transwell assays. The effect of HIF-1α expression on in vivo tumor metastasis of OSCC cells was evaluated using lung metastasis model. Results HIF-1α was overexpressed in patients with OSCC. OSCC metastasis was correlated with HIF-1α expression in OSCC tissues. Hypoxia increased the migration and invasion abilities of OSCC cell lines by regulating the expression and localization of partitioning-defective protein 3 (Par3) and TJs. Furthermore, HIF-1α silencing effectively decreased the invasion and migration abilities of OSCC cell lines and restored TJ expression and localization via Par3. The expression of HIF-1α was positively regulated the OSCC metastasis in vivo. Conclusions Hypoxia promotes OSCC metastasis by regulating the expression and localization of Par3 and TJ proteins. HIF-1α positively correlates to OSCC metastasis. Lastly, HIF-1α expression could regulate the expression of Par3 and TJs in OSCC. This finding may aid in elucidating the molecular mechanisms of OSCC metastasis and progression and developing new diagnostic and therapeutic approaches for OSCC metastasis.

show abstract

Section: Discussionmentioning

confidence: 99%

Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3

et al. 2023

Self Cite

View full text Add to dashboard Cite

show abstract

“…MicroRNAs (miRNAs) have become a research hotspot in malignant tumor research. The miRNAs are a group of small non-coding RNAs involved in regulating various biological processes such as cell proliferation, differentiation, migration and apoptosis, through interaction with specific genes [11]. Interestingly, miR-138, which is highly conserved in vertebrates, belongs to a class of miRNAs that participate in regulating cancer-related inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effect of miR-138 on migration and invasion of cervical cancer cells, and the underlying mechanism

Li,

Peng,

Huang

et al. 2023

Trop. J. Pharm Res

View full text Add to dashboard Cite

Purpose: To study the influence of microRNA-138 (miR-138) on the migration and invasion of cervical cancer cells, and the underlying mechanism. Methods: Fifteen cervical carcinoma subjects were enrolled in the study. Control group comprised cervical epithelial cell line (End1/E6E7) while cervical cancer group was human cervical squamous cell carcinoma cell line c33a. Both were cultured routinely without any treatment. In miR-138 overexpression group, cells were cultured in progeny of human cervical squamous carcinoma cell line c33a infected with miR-138 gene overexpression lentivirus. Expression levels of miR-138 in excised cervical cancer tissues were determined using qPCR. Cell proliferation was determined with CCK8 assay. Immunoblotting was utilized to assay protein expression levels. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine mRNA expression levels, while cell migration and invasion were assessed by Transwell method. Results: There was significant down-regulation of miR-138 expression in cervical cancer tissue, relative to nearby tissues (p < 0.05). In miR-138 overexpression group, cell proliferation, number of migrated and invaded cells were significantly reduced, relative to corresponding levels in cervical cancer cells. There were significantly higher expression levels of apoptosis-related proteins FAS, Bax and FasL in miR-138 overexpression group than in cervical cancer cells, while Bcl-2 was significantly downregulated, relative to cervical cancer group (p < 0.05). In cervical cancer cells, mRNA and protein levels of SIRT1 and HIF-1α were significantly up-regulated, relative to corresponding control, but levels of HIF1α and miR-138 were significantly reduced in overexpression group when compared to cervical cancer group (p < 0.05). Conclusion: Up-regulating miR-138 in cervical cancer cells reduces HIF-1α through inhibition of SIRT1 signaling, resulting in suppression of multiplication, migration and invasion of cervical cancer cells, while enhancing apoptotic changes.

show abstract

“…Oral squamous cell carcinoma is the most frequent malignant tumor of the head and neck with potential for lymph node metastasis, deep invasion and high recurrence rate, which shows poor prognosis and high mortality [ 1 , 2 ]. Despite the constant progression of therapeutic approaches, the 5-year survival rate has stagnated at about 50% [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone

Luo,

Long,

Lou

et al. 2024

BMC Oral Health

View full text Add to dashboard Cite

Background Chronic restraint stress (CRS) has iteratively been reported to be possibly implicated in the development of numerous cancer types. However, its role in oral squamous cell carcinoma (OSCC) has not been well elucidated. Here we intended to evaluate the role and mechanism. Methods The effects of CRS were investigated in xenograft models of OSCC by using transcriptome sequencing, LC–MS, ELISA and RT-PCR. Moreover, the role of CRS and ALDH3A1 on OSCC cells was researched by using Trans-well, flow cytometry, western blotting, immunofluorescence, ATP activity and OCR assay. Furthermore, immunohistochemical staining was employed to observe the cell proliferation and invasion of OSCC in xenotransplantation models. Results CRS promoted the progression of OSCC in xenograft models, stimulated the secretion of norepinephrine and the expression of ADRB2, but decreased the expression of ALDH3A1. Moreover, CRS changed energy metabolism and increased mitochondrial metabolism markers. However, ALDH3A1 overexpression suppressed proliferation, EMT and mitochondrial metabolism of OSCC cells. Conclusion Inhibition of ALDH3A1 expression plays a pivotal role in CRS promoting tumorigenic potential of OSCC cells, and the regulatory of ALDH3A1 on mitochondrial metabolism may be involved in this process.

show abstract

MicroRNA-18a regulates the metastatic properties of oral squamous cell carcinoma cells via HIF-1α expression

Cited by 12 publications

References 52 publications

Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3

Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3

Effect of miR-138 on migration and invasion of cervical cancer cells, and the underlying mechanism

Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone

Contact Info

Product

Resources

About