Reduced miR‑202 levels enhanced oral cancer development via targeting Sp1

Zhao, Jia; Ding, Deguang; Zhao, Ge

doi:10.3892/etm.2019.7603

Cited by 4 publications

(6 citation statements)

References 27 publications

(29 reference statements)

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“…In previous studies, miR-202 also was found to be aberrantly expressed in endometrial tissues from patients with EMS ( 13 , 38 ). In addition, miR-202 has been previous shown to exert suppressive roles on the invasive and migratory capacities of tumor cells ( 43 - 45 ). According to the aforementioned findings from the present and previous studies, it could be hypothesized that miR-202 can regulate EMS progression.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway

et al. 2020

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The enhanced migratory ability of endometrial stromal cells (ESCs) is a key factor in the formation of functional endometrium-like tissues outside the uterine cavity during endometriosis (EMS). Although accumulating evidence has suggested the importance of microRNAs (miRNAs) in the pathogenesis of EMS, the role of particular miRNAs in the invasiveness of ESCs remain poorly understood. In the present study, the function of miRNAs in the invasiveness of ESCs, along with the associated underlying mechanism involved, were investigated. Initially, the expression patterns of miRNAs in the ectopic and eutopic endometrium isolated from patients with EMS were analyzed using microarray. MicroRNA-202-5p (miR-202) was selected for further study due to its previously reported suppressive effects on the invasion in various types of cancers. The expression of miR-202 and K-Ras in eutopic and ectopic endometrioma tissues were detected using reverse transcription-quantitative PCR, immunohistochemistry and western blotting. The migration and invasion ability of ESCs was determined using wound healing and Transwell invasion assays, respectively. Compared with that from healthy individuals, miR-202 expression was demonstrated to be lower in the eutopic endometrium from patients with EMS, which was even lower in ectopic endometrium. Functional experiments in primary ESCs revealed that enhanced miR-202 expression suppressed the cell invasion and migration abilities, which was also accompanied with increased E-cadherin and reduced N-cadherin expression in ESCs, suggesting its potentially suppressive role in epithelial-mesenchymal transition. K-Ras is a well-known regulator of the ERK signaling pathway that was shown to be directly targeted and negatively regulated by miR-202. In addition, K-Ras expression was found to be upregulated in the ectopic endometrium, where it correlated negatively with that of miR-202. Knocking down K-Ras expression mimicked the anti-invasive effects of miR-202 overexpression on ESCs, whilst K-Ras overexpression attenuated the inhibitory role of miR-202 overexpression in ESC invasion. The K-Ras/Raf1/MEK/ERK signaling pathway was also blocked by miR-202 overexpression. These findings suggested that miR-202 inhibited ESC migration and invasion by inhibiting the K-Ras/Raf1/MEK/ERK signaling pathway, rendering miR-202 a candidate for being a therapeutic target for EMS.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway

et al. 2020

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“…On the other hand, in early-stage BC patients, a gradual decrease in miR-202 blood expression level was found to correlate with progression from early stage to tumor-node-metastasis (TNM) stage [ 11 ]. Similarly, a study on oral cancer reported decreased miR-202 levels in patient sera and cancer tissues [ 12 ].…”

Section: Circulating Mir-202 As a Diagnostic Biomarker In Cancer Pati...mentioning

confidence: 99%

“…Numerous clinical studies have addressed the role of miR-202 in gastrointestinal tract tumors (GIT), including oral [ 12 ], esophageal [ 19 , 20 , 21 ], gastric [ 22 , 23 , 24 ], pancreatic [ 25 , 26 , 27 , 28 ], hepatocellular [ 29 , 30 , 31 ], and colorectal [ 32 , 33 , 34 , 35 ] cancers, and documented a lower expression of miR-202 in tumor tissues and a tumor suppressive function of miR-202 overexpression on GIT cancer progression. In oral cancer cell lines, overexpression of miR-202 downregulated the protein expression level of the transcription factor Sp1, which, in turn, reduced cancer cell migration and invasion.…”

Section: Mir-202 As a Novel Gastrointestinal Tract Tumor Suppressormentioning

confidence: 99%

The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor

Ahmed

Rajendran

Scherthan

2022

IJMS

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MicroRNA-202 (miR-202) is a member of the highly conserved let-7 family that was discovered in Caenorhabditis elegans and recently reported to be involved in cell differentiation and tumor biology. In humans, miR-202 was initially identified in the testis where it was suggested to play a role in spermatogenesis. Subsequent research showed that miR-202 is one of the micro-RNAs that are dysregulated in different types of cancer. During the last decade, a large number of investigations has fortified a role for miR-202 in cancer. However, its functions can be double-edged, depending on context they may be tumor suppressive or oncogenic. In this review, we highlight miR-202 as a potential diagnostic biomarker and as a suppressor of tumorigenesis and metastasis in several types of tumors. We link miR-202 expression levels in tumor types to its involved upstream and downstream signaling molecules and highlight its potential roles in carcinogenesis. Three well-known upstream long non-coding-RNAs (lncRNAs); MALAT1, NORAD, and NEAT1 target miR-202 and inhibit its tumor suppressive function thus fueling cancer progression. Studies on the downstream targets of miR-202 revealed PTEN, AKT, and various oncogenes such as metadherin (MTDH), MYCN, Forkhead box protein R2 (FOXR2) and Kirsten rat sarcoma virus (KRAS). Interestingly, an upregulated level of miR-202 was shown by most of the studies that estimated its expression level in blood or serum of cancer patients, especially in breast cancer. Reduced expression levels of miR-202 in tumor tissues were found to be associated with progression of different types of cancer. It seems likely that miR-202 is embedded in a complex regulatory network related to the nature and the sensitivity of the tumor type and therapeutic (pre)treatments. Its variable roles in tumorigenesis are mediated in part thought its oncogene effectors. However, the currently available data suggest that the involved signaling pathways determine the anti- or pro-tumorigenic outcomes of miR-202’s dysregulation and its value as a diagnostic biomarker.

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“…Overexpression of SP1 has been observed in HNSCC as compared to normal oral mucosa, and its inhibition downregulates growth in oral cancer cell lines ( Shin et al, 2013 ). SP1 serves as a therapeutic target against oral cancer ( Shin et al, 2012 ; Yu et al, 2013 ; Chae et al, 2014 ; Sun et al, 2016 ; Zhang et al, 2019 ; Zhao et al, 2019 ; Gao et al, 2020 ; Liu et al, 2020 ). SP1 is a functional target of miR-24.…”

Section: Role Of Hpv-related Transcription Factors In Handn Carcinogenementioning

confidence: 99%

Human Papillomavirus Infection in Head and Neck Squamous Cell Carcinomas: Transcriptional Triggers and Changed Disease Patterns

Aggarwal

Yadav

Thakur

et al. 2020

Front. Cell. Infect. Microbiol.

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Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous group of cancers. Collectively, HNSCC ranks sixth in incidence rate worldwide. Apart from classical risk factors like tobacco and alcohol, infection of human papillomavirus (HPV) is emerging as a discrete risk factor for HNSCC. HPV-positive HNSCC represent a distinct group of diseases that differ in their clinical presentation. These lesions are well-differentiated, occur at an early age, and have better prognosis. Epidemiological studies have demonstrated a specific increase in the proportions of the HPV-positive HNSCC. HPV-positive and HPV-negative HNSCC lesions display different disease progression and clinical response. For tumorigenic-transformation, HPV essentially requires a permissive cellular environment and host cell factors for induction of viral transcription. As the spectrum of host factors is independent of HPV infection at the time of viral entry, presumably entry of HPV only selects host cells that are permissive to establishment of HPV infection. Growing evidence suggest that HPV plays a more active role in a subset of HNSCC, where they are transcriptionally-active. A variety of factors provide a favorable environment for HPV to become transcriptionally-active. The most notable are the set of transcription factors that have direct binding sites on the viral genome. As HPV does not have its own transcription machinery, it is fully dependent on host transcription factors to complete the life cycle. Here, we review and evaluate the current evidence on level of a subset of host transcription factors that influence viral genome, directly or indirectly, in HNSCC. Since many of these transcription factors can independently promote carcinogenesis, the composition of HPV permissive transcription factors in a tumor can serve as a surrogate marker of a separate molecularly-distinct class of HNSCC lesions including those cases, where HPV could not get a chance to infect but may manifest better prognosis.

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Reduced miR‑202 levels enhanced oral cancer development via targeting Sp1

Cited by 4 publications

References 27 publications

MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway

MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway

The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor

Human Papillomavirus Infection in Head and Neck Squamous Cell Carcinomas: Transcriptional Triggers and Changed Disease Patterns

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