Expression and Prognostic Implications of FOXO3a and Ki67 in Lung Adenocarcinomas

Liu, Hongbin; Gao, Xiang-Xiang; Zhang, Qing; Liu, Jian; Yuan, Cui; Zhu, Yan; Liu, Yifei

doi:10.7314/apjcp.2015.16.4.1443

Cited by 15 publications

(16 citation statements)

References 24 publications

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“…Ki-67 is involved in maintaining the structure of the stable DNA in mitosis and has been used as an indicator of the proliferation rate in a number of human malignancies ( 12 ). Various studies have shown that the level of Ki-67 is closely associated with the development and progression of a variety of cancer types, including lung adenocarcinoma, breast cancer, adrenocortical carcinoma and gastric cancer ( 13 – 16 ). In laryngeal carcinoma, however, there is no consensus on the role of Ki-67.…”

Section: Discussionmentioning

confidence: 99%

Ki-67 is overexpressed in human laryngeal carcinoma and contributes to the proliferation of HEp2 cells

Bai

Shao

et al. 2016

Oncology Letters

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Ki-67 is one of the most useful markers to evaluate cell proliferative activity and has been widely used in tumor treatment and research. However, its role in human laryngeal carcinoma remains poorly defined. The aim of the present study was to investigate the expression of Ki-67 in human laryngeal squamous carcinoma and the effect of Ki-67 gene silencing by small interfering (si)RNA on the proliferation of human laryngocarcinoma HEp2 cells. Immunohistochemistry and reverse transcription-quantitative polymerase chain reaction were performed to examine the expression of Ki-67 in human laryngeal squamous carcinoma tissues and adjacent non-cancer tissues from 50 patients with laryngeal squamous carcinoma. RNA interference was used to knock down the expression of Ki-67 in the HEp2 cell line, and the proliferation of the treated cells was observed in vitro. Western blot analysis was used to determine the expression levels of epidermal growth factor receptor (EGFR) and E-cadherin in the treated cells. The expression of Ki-67 in the laryngeal squamous carcinoma tissues was significantly higher than that of the adjacent non-tumor tissues (P=0.028). The high expression of Ki-67 in cancer was significantly correlated with cervical lymph node metastasis and clinical outcomes (all P<0.001). The silencing of Ki-67 resulted in the inhibition of proliferation of the HEp2 human laryngocarcinoma cells (P<0.001). In addition, compared with the control group, the expression levels of EGFR and E-cadherin in the Ki-67 siRNA-treated cells were significantly decreased (P<0.001) and increased (P<0.001), respectively. These results suggested that Ki-67 is important in regulating the proliferation of human laryngocarcinoma HEp2 cells and that the mechanism may at least partially be associated with the upregulation of EGFR and the downregulation of E-cadherin. Overall, Ki-67 can be used as an important indicator for judging clinical progress and estimating prognosis in human laryngeal squamous carcinoma.

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Section: Discussionmentioning

confidence: 99%

Ki-67 is overexpressed in human laryngeal carcinoma and contributes to the proliferation of HEp2 cells

Bai

Shao

et al. 2016

Oncology Letters

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“…FOXO3 is a member of the forkhead transcription factors and is characterized by a unique forkhead domain . The abnormal expression of FOXO3 is obviously correlated with the occurrence and development of tumors . The 3'‐UTR of FOXO3 has two sequence‐conserved binding sites for miRNA‐96, which inhibits the expression of FOXO3 after binding .…”

Section: Introductionmentioning

confidence: 99%

“…11 The abnormal expression of FOXO3 is obviously correlated with the occurrence and development of tumors. 12 The 3'-UTR of FOXO3 has two sequenceconserved binding sites for miRNA-96, which inhibits the expression of FOXO3 after binding. 13 Iwai et al confirmed that miRNA-96 is highly expressed in human hepatocellular carcinoma, and inhibiting miRNA-96 can increase the expression levels of FOXO1 and FOXO3, thereby reducing the proliferation and colony formation of hepatoma cell lines.…”

Section: Introductionmentioning

confidence: 99%

MiRNA‐96‐5p impacts the progression of breast cancer through targeting FOXO3

Yin

Wang

et al. 2020

Thoracic Cancer

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Background Breast cancer is the most common malignant tumor in women worldwide, with a high mortality rate. MicroRNAs are small non‐coding RNAs that negatively regulate the expression of target genes by interacting with the target gene 3'‐UTR, and participate in cell differentiation, proliferation, apoptosis and metabolism. The function of miRNA‐96‐5p in the progression of breast cancer has not been reported. Methods We used the StarBase database to investigate the expression of miRNA‐96‐5p in breast cancer and adjacent normal tissues. FOXO3 3'‐UTR construct and luciferase reporter assays was performed for the target gene. Expression levels of miRNAs including its target were analyzed by qRT‐PCR and western blot. Cell proliferation was detected by CCK8 and colony formation, EdU assay. Results Luciferase reporter assays showed miRNA‐96‐5p directly targeted FOXO3. Abrogation of miRNA‐96‐5p by transfection with its inhibitors in breast cancer cells significantly suppressed miRNA‐96‐5p expression and breast cancer cells proliferation. Western blot revealed that overexpression of miRNA‐96‐5p substantially reduced FOXO3 protein expression. We used the GEPIA, UALCAN and KM‐plotter databases to investigate the expression of FOXO3 in human breast cancer and adjacent normal tissues, and its correlation with survival. In addition, we found that FOXO3 spoiled miR‐96‐5p induced breast cancer cell proliferation block effecting. Conclusions miRNA‐96‐5p may exert a tumor promotion role through negatively regulating tumor suppressor gene FOXO3 and promoting cell proliferation.

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“…Next, we investigated the possible targets of miR-122-5p and identified FOXO3 as a likely candidate. FOXO3 is a critical protein involved in cell cycle arrest and apoptosis (16,17). Therefore, FOXO3 is recognized as a tumor suppressor, and decreased FOXO3 expression is associated with progression of various tumors, including GC (18)(19)(20).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of apoptosis by miR‑122‑5p in α‑fetoprotein‑producing gastric cancer

et al. 2019

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α-Fetoprotein (AFP)-producing gastric cancer (AFPGC) is recognized as one of the most aggressive tumors with subsequent poor prognosis compared with common gastric cancer (GC) subtypes. However, the molecular mechanism remains to be elucidated. We previously identified that miR-122-5p could be a useful biomarker in AFPGC patients. We examined herein the biological function of miR-122-5p and the molecular mechanism underlying tumor progression in AFPGC. We used the AFPGC cell line (FU97) and miR-122-5p inhibitor to examine the function of miR-122-5p. Moreover, we investigated the possible targets of miR-122-5p. The expression level of miR-122-5p was significantly increased in the FU97 cell line than in common GC cell lines. Also, suppression of miR-122-5p significantly reduced AFP levels and proliferation in AFPGC through an induction of apoptosis. Western blotting revealed that the expression of anti-apoptotic protein (Bcl-2) was decreased and that of pro-apoptotic protein (caspase-3) was increased in miR-122-5p suppression of FU97. Moreover, we revealed that FOXO3 was an important target of miR-122-5p in AFPGC, which inhibited apoptosis and subsequently manifested aggressiveness. In conclusion, miR-122-5p inhibited apoptosis and facilitated tumor progression by targeting FOXO3 in AFPGC, which indicates the possibility of miR-122-5p as a potential therapeutic target in AFPGC.

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Expression and Prognostic Implications of FOXO3a and Ki67 in Lung Adenocarcinomas

Cited by 15 publications

References 24 publications

Ki-67 is overexpressed in human laryngeal carcinoma and contributes to the proliferation of HEp2 cells

Ki-67 is overexpressed in human laryngeal carcinoma and contributes to the proliferation of HEp2 cells

MiRNA‐96‐5p impacts the progression of breast cancer through targeting FOXO3

Inhibition of apoptosis by miR‑122‑5p in α‑fetoprotein‑producing gastric cancer

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