miR-106a Regulates Cell Proliferation and Autophagy by Targeting LKB1 in HPV-16–Associated Cervical Cancer

Cui, Xiujie; Xiao, Wang; Zhou, Xin; Jia, Jihui; Chen, Hanxiang; Zhao, Weiming

doi:10.1158/1541-7786.mcr-19-1114

Cited by 37 publications

(27 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After further analyzing the cancer-promoting mechanism of miR-106a-5p, it was demonstrated that miR-106a-5p targeted and inhibited LKB1 levels. A recent study indicated that in HPV-16-associated cervical cancer, LKB1 regulated proliferation and autophagy, and its expression level was targeted by miR-106a (49). In the present study, overexpression of LKB1 inhibited the proliferation and migration, and promoted autophagy of Calu-3 and NCI-H661 cells.…”

Section: Discussionsupporting

confidence: 61%

MicroRNA‑106a‑5p promotes the proliferation, autophagy and migration of lung adenocarcinoma cells by targeting LKB1/AMPK

Zhou

Zhang

et al. 2021

Exp Ther Med

View full text Add to dashboard Cite

It has previously been reported that lung cancer has the highest morbidity and mortality rate worldwide; however, the pathogenesis underlying lung cancer has not been fully elucidated. The aim of the present was primarily to assess the influence of microRNA (miR)-106a-5p on the biological behaviors of lung cancer cells. In the present study, bioinformatics analysis was used to analyze the expression characteristics of miR-106a-5p and its relationship with the prognosis of patients with lung adenocarcinoma (LUAD) in The Cancer Genome Atlas. A dual luciferase reporter assay was performed to verify the binding of miR-106a-5p and liver kinase B1 (LKB1). The Cell Counting Kit-8, colony formation and Transwell assays were utilized to detect cell viability, proliferation and migration, respectively. Protein and RNA expression levels were examined by western blotting and reverse transcription-quantitative PCR analysis, respectively. It was observed that miR-106a-5p was highly expressed in LUAD and associated with poor prognosis. miR-106a-5p promoted the proliferation and migration of LUAD cells, and inhibited autophagy. By contrast, LKB1 inhibited cell proliferation and migration, promoted autophagy and blocked the cancer-promoting effects of miR-106a-5p. Overexpression of miR-106a-5p inhibited the phosphorylation of AMP-activated protein kinase (AMPK) and tuberin (TSC2), and promoted the phosphorylation of mTOR. By contrast, overexpression of LKB1 blocked the promotion of mTOR phosphorylation, and the inhibition of AMPK and TSC2 phosphorylation caused by miR-106a-5p. In summary, the results of the present study indicated that miR-106a-5p regulated the phosphorylation of the AMPK pathway by targeting LKB1, and was involved in the proliferation, migration and autophagy of LUAD cells.

show abstract

Section: Discussionsupporting

confidence: 61%

MicroRNA‑106a‑5p promotes the proliferation, autophagy and migration of lung adenocarcinoma cells by targeting LKB1/AMPK

Zhou

Zhang

et al. 2021

Exp Ther Med

View full text Add to dashboard Cite

show abstract

“…Activation of Akt can activate the downstream mTOR, thereby reducing the expression of Beclin-1 and LC3 and inhibiting autophagy. Studies have shown that DDP can activate Akt/mTOR pathway and cause drug resistance in bladder cancer, ovarian cancer and nasopharyngeal carcinoma [18] . PI3K/Akt/mTOR signaling pathway can stimulate cell growth in multiple stages of cell cycle.…”

Section: Resultsmentioning

confidence: 99%

Exploring the Mechanism of MicroRNA-125a Reversing the Resistance of Laryngeal Cancer Stem Cells to Cisplatin from Mitochondrial Autophagy

Liu¹,

Meng²,

Li³

2021

ijps

View full text Add to dashboard Cite

To explore the mechanism of microRNA-125a reversing the resistance of laryngeal cancer stem cells to cisplatin from mitochondrial autophagy. The human laryngeal carcinoma cell line Hep-2 was purchased from Shanghai Bioleaf Biotechnology Co., Ltd. The expression of microRNA-125a messenger RNA in each group of cells was analyzed by reverse transcription-polymerase chain reaction. The cell migration and invasion ability of each group was evaluated by Transwell assay. Cell apoptosis was detected by flow cytometry. Western blot analysis was conducted to evaluate the protein expression. The expression of microRNA-125a messenger RNA in the Hep-2/diamminedichloroplatinum group was lower than that in the control group (p<0.05) and the expression of microRNA-125a messenger RNA in the microRNA-125a mimic group was higher than that in the Hep-2/diamminedichloroplatinum group (p<0.05). Compared with the Hep-2/diamminedichloroplatinum group, the microRNA-125a mimic group had more mitochondrial fragments and the average branch length of mitochondria decreased (p<0.05). The cell migration, invasion and viability of the Hep-2/diamminedichloroplatinum group increased (p<0.05) and the apoptosis rate decreased (p<0.05). The protein expression of phosphoinositide 3-kinase, protein kinase B and mammalian target of rapamycin in the Hep-2/diamminedichloroplatinum group was higher than that in the control group (p<0.05) and their expression in the microRNA-125a mimic group was lower than that in the Hep-2/ diamminedichloroplatinum group (p<0.05). The dysregulation of microRNA-125a was related to diamminedichloroplatinum resistance in laryngeal cancer and diamminedichloroplatinum resistance was induced by microRNA-125a through phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway mediated autophagy inhibition. Overexpression of microRNA-125a inhibited the growth and metastasis of Hep-2/diamminedichloroplatinum cells through the phosphoinositide 3-kinase/ protein kinase B/mammalian target of rapamycin pathway and induced their apoptosis and autophagy.

show abstract

“…MiR-106a-5p was reported to be dysregulated in various of diseases, such as prostate cancer (23), atherosclerosis (24) and cervical cancer (25). The clinical value of miR-106a-5p in diseases attracted researcher attention.…”

Section: Discussionmentioning

confidence: 99%

“…As reported by Zhang et al, miR-106a-5p level was downregulated in osteoarthritis (OA) samples and IL-1b-treated chondrocytes, miR-106a-5p overexpression led to proliferation promotion and apoptosis inhibition in chondrocytes treated by IL-1β (26). Another study in HPV-16-associated cervical cancer reported that miR-106a-5p played an important role in regulatory mechanism of cervical squamous cell carcinoma (CSCC) and could be a potential therapeutic target in HPV-associated cervical cancer (25). Considering the dysregulation of miR-106a-5p in the serum of psoriasis patients, we further explored whether serum miR-106a-5p could differentiate between the psoriasis patients and the healthy.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic value of miR-106a-5p in patients with psoriasis and its regulatory role in inflammatory responses

Miao

Tong

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Psoriasis is a multifactorial, recurring, and chronic inflammatory skin disease. This study was designed to explore the potential role of microRNA-106a-5p (miR-106a-5p) in psoriasis.Methods: The expression levels of miR-106a-5p in the serum of psoriasis patients and healthy individuals were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The diagnostic value of miR-106a-5p in serum was evaluated by the receiver operating characteristics curve (ROC). The levels of interleukin-22 (IL-22), interleukin-17A (IL-17A), and tumor necrosis factor-alpha (TNF-alpha) were determined by enzyme-linked immunosorbent assay.Results: The serum expression of miR-106a-5p was found to be up-regulated in psoriasis patients. ROC curve showed that miR-106a-5p had high specificity and sensitivity in the diagnosis of psoriasis. The correlation between the serum expression level of miR-106a-5p and PASI was positive. The relative expression levels of IL-17A, IL-22 and TNF-alpha in serum of psoriasis patients were significantly upregulated compared with that in healthy control, and showed positive association with serum miR-106a-5p levels. Cell experiments demonstrated that upregulation of miR-106a-5p could promote cell proliferation, and the levels of IL-22, IL-17A and TNF-alpha were upregulated significantly in M5-induced HaCaT cells.Conclusion: Considering the novel and vital role in psoriasis progression, miR-106a-5p is expected to be a new potent target for treatment of psoriasis. MiR-106-5p was expected to use for more immunity diseases research and therapy.

show abstract

miR-106a Regulates Cell Proliferation and Autophagy by Targeting LKB1 in HPV-16–Associated Cervical Cancer

Cited by 37 publications

References 41 publications

MicroRNA‑106a‑5p promotes the proliferation, autophagy and migration of lung adenocarcinoma cells by targeting LKB1/AMPK

MicroRNA‑106a‑5p promotes the proliferation, autophagy and migration of lung adenocarcinoma cells by targeting LKB1/AMPK

Exploring the Mechanism of MicroRNA-125a Reversing the Resistance of Laryngeal Cancer Stem Cells to Cisplatin from Mitochondrial Autophagy

Diagnostic value of miR-106a-5p in patients with psoriasis and its regulatory role in inflammatory responses

Contact Info

Product

Resources

About