miR-100 expression

In certain oncogenic capacities, the lncRNA MIR100HG functions as a competitive endogenous RNA for miR-136-5p, hence impeding the inhibitory effect of miR-136-5p on its target gene, IL-6. In summary, the findings of the present investigation suggested that lncRNA MIR100HG exhibits promising characteristics as a potential indicator for the prognosis and diagnosis of NPC.

Collectively, our study provides evidence that sevoflurane restrained the proliferation and invasion in lung cancer cells by modulating the miR-100-3p/SOAT1 axis. This article provides a new idea for further study of the pathogenesis of lung cancer.

OS and DFS worsened in DM subjects with both HbA1c ≥ 6.5% and DM duration ≥3 years. Thus, DM is associated with two modes of epigenetic change by independent mechanisms and worsens prognosis.

The current preliminary research reveals serum hsa_circ_0072309 as a possible biomarker and target for early diagnosis, prognosis, and therapy of NSCLC-derived BM and suggests a substantial role for the hsa_circ_0072309/miR-100/ACKR3 axis in the formation of BM from NSCLC.

Western-blot analysis showed that PTCSC3 suppressed viability and promoted apoptosis of TNBC cells through the Hippo signaling pathway. Thus, the present study demonstrated that lncRNA PTCSC3 inhibits cancer cell viability and promotes cancer cell apoptosis in TNBC by downregulating MIR100HG.

To better understand the importance of miRNAs in OSCC, various OSCC cases were analyzed. Detecting miRNAs in plasma may be a useful diagnostic tool for oral squamous cell carcinoma.

We also discovered that overexpression of miR-100 induces paclitaxel resistance, thereby reducing the drug's therapeutic effect on cell death. Our results are consistent with the hypothesis that cervical cancer cells overexpress miR-100 in response to hypoxia and that miR-100 is a facilitator of USP15 downregulation and inactivation.

Moreover, in the collected samples, miR-100-5p was lowly expressed in PTC tissues compared with normal tissues, especially in those of advanced stage (Stage III/IV vs Stage I/II), while FZD8 was highly expressed in PTC tissues, which in PTC tissues was inversely correlated to miR-100-5p. Thus, we suggest that overexpression of miR-100-5p inhibits the development of PTC by targeting FZD8.

These results conclude that HAGLROS is a tumor promoter in NSCLC, and it regulates the malignant phenotypes of NSCLC cells via miR-100/SMARCA5 axis.

The conclusions indicate miR-100 is a tumor suppressor gene and could be a therapeutic target in radio-resistant cervical cancers.

MIR100HG and hnRNPA2B1 interact to control the transcriptional activity of Wnt signaling in CRC via regulation of TCF7L2 mRNA stability. Our findings identified MIR100HG as a potent EMT inducer in CRC that may contribute to cetuximab resistance and metastasis by activation of a MIR100HG/hnRNPA2B1/TCF7L2 feedback loop.

We have obtained a two-miRNA risk score model. Our results provide a new strategy for the individualized diagnosis and treatment of CC.

MIR100HG regulates CALD1 expression by targeting miR-142-5p to inhibit the proliferation, migration and invasion of bladder cancer cells. MIR100HG is an independent prognostic factor for bladder cancer, with potential as a biomarker for the diagnosis and treatment of bladder cancer.

HAGLROS overexpression contributes to DLBCL development and poor prognosis via targeting miR-100, which could be a potential prognostic biomarker and therapeutic target for DLBCL patients.

We then evaluated expression of these core microRNAs in pre-PD-1-inhibitor-treated melanoma patients and observed that higher expression of miR-100-5p and miR-125b-5p were associated with significantly improved overall survival. These findings suggest that miR-100-5p and 125b-5p are potential markers of response to PD-1 inhibitors, and further evaluation of these microRNA-mRNA interactions may yield further insight into melanoma resistance to PD-1 inhibitors.

Taken together, the results of the present study suggest that miR-100 inhibits the proliferation, migration and invasion of breast cancer cells by targeting FOXA1 expression. These results may provide a novel insight and an experimental basis for identifying effective therapeutic targets of high specificity for breast cancer.

Moreover, miR-146b-5p suppression or CBX6 elevation evidently rescued the suppressed viability, migration, and invasion of HCC cells caused by MIR100HG knockdown. Knockdown of MIR100HG inhibited the viability, migration, and invasion of HCC cells by targeting the miR-146b-5p/CBX6 axis, offering a potential therapeutic target for HCC therapy.

Serum miR-100 may be a useful diagnostic biomarker for CC, and for predicting lymph node metastasis and disease free survival in CC patients.

Conclusively, miR-100 exerts antitumor effects on hepatocellular carcinoma. Overexpression of miR-100 attenuates the invasive and proliferative abilities of hepatocellular carcinoma cells by targeting CXCR7.

Gene expression of these cells showed increased expression of ZBED2, ZBTB20, ABCC3, UHMK1, and low expression of Transgelin and MARCKS. We present evidence that ovarian ascitic EVs increase the growth of ovarian cancer spheroids through miRNAs.

Meanwhile, the identified differentially expressed exosome-miRNAs may partially associate with tumorigenesis. To sum up, the identified exosome-miRNAs may play role in the development of lung cancer induced by chronic PM2.5 exposure.