Notch1 targeted regulation of mir-224/LRIG2 signaling for the proliferation and apoptosis of cervical cancer cells

Abstract

In the present study, we explored the participation of Notch1 targeted regulation of mir-224/LRIG2 gene signal pathway in proliferation and apoptosis of cervical cancer cells. Forty-nine cases of cervical cancer lesion samples from cervical cancer patients treated in our hospital from February 2013 to February 2015 were chosen as subjects (the observation group), and cervical samples of healthy women (42 cases) during the same period were used as the control group. We determined the mRNA and protein expression of Notch1, mir-224, and LRIG2 genes. We also analyzed the mutual relationship between Notch1 gene expression and cervical cancer. The Notch1 genes in the cervical cancer cells (HeLa) were silenced and overexpressed to measure cancer apoptosis with flow cytometry. After obstruction of the Notch1 signal pathway, the mRNA and protein expression in the mir-224 and LRIG2 genes was also measured. It was found that in comparison to the control group, Notch1 gene expression in the observation group was significantly higher (p<0.05), cell growth was suppressed in Notch1 silent cell strains but accelerated in overexpressed Notch1 cells. The silencing of Notch1 genes can lead to the reduction of mir-224/LRIG gene and protein levels, while overexpression of the Notch1 genes increased the mir-224/LRIG gene and protein levels. In conclusion, the Notch1 gene is positively related to cervical cancer and can promote the occurrence of the disease. The potential mechanism shows that Notch1 gene can regulate cervical cancer cell proliferation by regulating the mir-224/LRIG2 signal pathway.

Mifepristone Inhibits the Migration of Cervical Cancer Cells by Inhibiting Exocrine Secretion

“…For example, The Notch1 gene is reported to be related to CC as well as promote the occurrence of this disease. The potential mechanism shows that Notch1 regulates the proliferation of CC cells by regulating the mir-224/LRIG2 signal pathway [20]. In addition, sulfiredoxin was demonstrated to be an oncoprotein in CC and promote CC metastasis by activating the Wnt/β-catenin signaling.…”

MLK3 silence induces cervical cancer cell apoptosis via the Notch‐1/autophagy network

“…Notch‐1 signalling participates in tumourigenesis, chemoresistance, cancer cell growth, and metastasis . It is elevated in organ‐specific cancers, including gynaecological malignancies . Accumulating data has suggested that Notch‐1 is implicated in autophagy and plays a critical role in cervical cancer .…”

“…In murine natural T‐regulatory cells, Notch‐1 regulated autophagy controls survival and suppressor activity of these cells . Additionally, Cong et al show that Notch‐1 gene expression is significantly higher in patients with cervical cancer lesions than it is in normal humans, and silencing of Notch‐1 suppresses cell growth. Consistent with previous reports, expression of Notch‐1 was higher in cervical cancer cell lines than in the control H8 cells.…”

“…25 It is elevated in organ-specific cancers, including gynaecological malignancies. 26,27 Accumulating data has suggested that Notch-1 is implicated in autophagy and plays a critical role in cervical cancer. 21,28,29 In stem cell development and neurogenesis, autophagy degrades Notch-1, which correlates with Notch hyperactivity.…”

Upregulated expression of HOXC8 is associated with poor prognosis of cervical cancer

“…Additionally, the molecular mechanisms underlying the development of CC remain poorly understood. Previous studies have demonstrated that aberrant expression of several proteins is associated with the proliferation and apoptosis of CC cell lines (5,6). Therefore, the identification of genetic alterations that may be associated with the progression of CC may provide insights for the development of novel therapeutic strategies.…”