GRHL3 Promotes Tumor Growth and Metastasis via the MEK Pathway in Colorectal Cancer

Abstract

GRHL3 is a factor associated with a tumor, of which the molecular mechanism remains a further investigation. We explored the underlying mechanism of tumor-promoting effect of GRHL3 in colorectal cancer (CRC), which is involved in the MEK1/2 pathway. The expression of GRHL3 was measured in CRC and adjacent normal tissue using qPCR and immunohistochemical staining. Lentivirus-mediated knockdown expression of GRHL3 was performed in the CRC cell line HT29. Cell proliferation and metastasis were assayed in vitro, and tumorigenicity was investigated in vivo. We found higher GRHL3 expression in colorectal cancer, which was negatively correlated with patients’ prognosis. Results from studies in vitro and in vivo indicated that downregulation of GRHL3 expression inhibited tumor growth and metastasis and inhibited the activation of the MEK1/2 pathway. The effect of GRHL3 downexpression was the same as that of MEK1/2 antagonists on suppression of tumor growth and metastasis. Our results suggested that GRHL3 may act as an oncogene to promote tumor growth and metastasis via the MEK pathway in colorectal cancer.

NIFK as a potential prognostic biomarker in colorectal cancer correlating with immune infiltrates

“…102 CRC tissue samples (38 rectal cancer and 64 colon cancer) with clinical features including gender, age, tumor size, tumor-node-metastasis stage, degree of differentiation and regional lymph node metastasis and 30 para-carcinoma tissue samples (10 rectum and 20 colon) were collected in the Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University with informing consent according to our previous study. [ 19 ] This study was approved by the ethics committee of the he Affiliated Zhuzhou Hospital Xiangya Medical College CSU (No. : 2018K0327), and all patients signed an informed consent form.…”

“…After then, qRT-PCR was performed using a SYBR green PCR kit (Qiagen) on the iCycler iQ (Bio-RAD) according to our previous study. [ 19 ] The reaction program including pre-denaturation at 95°C for 10min as well as denaturation at 95°C for 10 seconds, annealing at 60°C for 30 seconds, extension at 72°C for 30 seconds involved in 45 cycles. β-actin was used to normalize target genes, the relative expression of which was obtained using 2 - Δ Δ CT method.…”

“…Protein expression and localization of NIFK were analyzed in all the samples collected from our hospital by IHC staining based on our previous study. [ 19 ] A mouse-anti NIFK monoclonal primary antibody (ab244216, Abcam, UK) was used to identified NIFK protein and then marked by second antibody conjugated with horseradish peroxidase (HRP). The nucleus was counterstained using hematoxylin.…”