<scp>DMBT1</scp> suppresses cell proliferation, migration and invasion in ovarian cancer and enhances sensitivity to cisplatin through galectin‐3/<scp>PI3k</scp>/Akt pathway

Ma, Nan; Zhao, Yuqing

doi:10.1002/cbf.3549

Cited by 11 publications

(9 citation statements)

References 28 publications

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“… 48 , 49 , 50 Deleted in malignant brain tumors 1 (DMBT1) overexpression induced the inactivation of PI3K/AKT pathway, thereby suppressing cisplatin resistance in OC. 51 Wogonin enhanced cisplatin sensitivity in OC by inhibition of PI3K/AKT pathway. 52 As for the correlation between RHPN1‐AS1 and PI3K/AKT pathway, only one article reported that RHPN1‐AS1 could activate PI3K/AKT pathway to promote the malignancy of hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

METTL3‐mediated m6A modification of lnc RNA RHPN1‐AS1 enhances cisplatin resistance in ovarian cancer by activating PI3K/AKT pathway

Cui

2022

Clinical Laboratory Analysis

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Background Cisplatin resistance is a big challenge for ovarian cancer (OC) therapy. The abnormal expression of long noncoding RNAs (lncRNAs) regulated by N6‐methyladenosine (m6A) modification has been confirmed to play the crucial roles in OC. The aim of this study is to explore the regulatory mechanism of lncRNA RHPN1‐AS1 on OC with cisplatin resistance. Methods The real‐time reverse transcription‐polymerase chain reaction was carried out to confirm the expression of RHPN1‐AS1 and methyltransferase‐like 3 (METTL3) in OC. The effects of RHPN1‐AS1 on cisplatin‐resistant OC cells were identified by cell functional experiments and animal experiment. Western blotting was performed to detect the effect of RHPN1‐AS1 on PI3K/AKT pathway. Moreover, methylated RNA immunoprecipitation and RNA stability assays confirmed the interaction between RHPN1‐AS1 and METTL3. Results RHPN1‐AS1 and METTL3 were confirmed to be overexpressed in OC. After transfecting RHPN1‐AS1 overexpression or RHPN1‐AS1 knockdown vectors into cisplatin‐resistant OC cells, it was found that upregulating RHPN1‐AS1 contributed to cell viability, migration, invasion, and tumor growth in vivo. In addition, RHPN1‐AS1 could enhance the protein levels of PI3K and phosphorylated AKT in cisplatin‐resistant OC cells, and METTL3 could enhance the stability of RHPN1‐AS1 by the m6A modification. Conclusion Overall, this study revealed that METTL3‐mediated m6A modification of RHPN1‐AS1 accelerates cisplatin resistance in OC by activating PI3K/AKT pathway.

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Section: Discussionmentioning

confidence: 99%

METTL3‐mediated m6A modification of lnc RNA RHPN1‐AS1 enhances cisplatin resistance in ovarian cancer by activating PI3K/AKT pathway

Cui

2022

Clinical Laboratory Analysis

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“…The DMBT1 gene encodes a protein involved in cell proliferation and is considered a tumor suppressor for the brain and epithelial cancer [ 82 – 85 ]. Some studies have shown conflicting results in reducing or increasing the expression of DMBT1 in various cancers [ 86 , 87 ].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of CSTB and DMBT1 expression in saliva of gastric cancer patients and controls

et al. 2022

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Background Gastric cancer (GC) is the fifth most common cancer and the third cause of cancer deaths globally, with late diagnosis, low survival rate, and poor prognosis. This case-control study aimed to evaluate the expression of cystatin B (CSTB) and deleted in malignant brain tumor 1 (DMBT1) in the saliva of GC patients with healthy individuals to construct diagnostic algorithms using statistical analysis and machine learning methods. Methods Demographic data, clinical characteristics, and food intake habits of the case and control group were gathered through a standard checklist. Unstimulated whole saliva samples were taken from 31 healthy individuals and 31 GC patients. Through ELISA test and statistical analysis, the expression of salivary CSTB and DMBT1 proteins was evaluated. To construct diagnostic algorithms, we used the machine learning method. Results The mean salivary expression of CSTB in GC patients was significantly lower (115.55 ± 7.06, p = 0.001), and the mean salivary expression of DMBT1 in GC patients was significantly higher (171.88 ± 39.67, p = 0.002) than the control. Multiple linear regression analysis demonstrated that GC was significantly correlated with high levels of DMBT1 after controlling the effects of age of participants (R2 = 0.20, p < 0.001). Considering salivary CSTB greater than 119.06 ng/mL as an optimal cut-off value, the sensitivity and specificity of CSTB in the diagnosis of GC were 83.87 and 70.97%, respectively. The area under the ROC curve was calculated as 0.728. The optimal cut-off value of DMBT1 for differentiating GC patients from controls was greater than 146.33 ng/mL (sensitivity = 80.65% and specificity = 64.52%). The area under the ROC curve was up to 0.741. As a result of the machine learning method, the area under the receiver-operating characteristic curve for the diagnostic ability of CSTB, DMBT1, demographic data, clinical characteristics, and food intake habits was 0.95. The machine learning model’s sensitivity, specificity, and accuracy were 100, 70.8, and 80.5%, respectively. Conclusion Salivary levels of DMBT1 and CSTB may be accurate in diagnosing GCs. Machine learning analyses using salivary biomarkers, demographic, clinical, and nutrition habits data simultaneously could provide affordability models with acceptable accuracy for differentiation of GC by a cost-effective and non-invasive method.

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“…Emerging research have claimed that most proteins require interacting with other proteins in the cell to function properly, and this interaction between proteins may influence each other and form a complex regulatory network, thus exerting important effects on the biological processes of various kinds of tumor cells [ 24 , 25 ]. For example, Ma N et al demonstrated that deleted in malignant brain tumors 1 (DMBT1) could interact with galectin-3 and exert suppressive effects on cell proliferation, migration and invasion in ovarian cancer cells through galectin-3-mediated PI3k/Akt signaling [ 26 ]. Cui H et al confirmed the interaction between DTL and programmed cell death 4 (PDCD4) by Co-IP assay, and revealed that DTL enhanced the motility and proliferation of cancer cells through degrading PDCD4, thus promoting cancer progression [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of KRAB domain-associated protein 1 suppresses the proliferation, migration and invasion of thyroid cancer cells by regulating P68/DEAD box protein 5

2022

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KRAB domain-associated protein 1 (KAP-1) has been reported to be an oncogene in diverse tumors. KAP-1 was found to have abundant existence in malignant thyroid tissues, but its role in thyroid cancer hasn’t been elucidated clearly. This study was carried out to explore the role of KAP-1 in thyroid cancer, and to clarify its molecular mechanism. The expressions of KAP-1 and P68/DEAD box protein 5 (DDX5) were assessed under the help of qRT-PCR and western blot. Then, we downregulated KAP-1 or upregulated DDX5 by cell transfection in TPC-1 cells. A series of cellular experiments on proliferation, apoptosis, migration and invasion were conducted with CCK-8, EdU, TUNEL, wound-healing and Transwell assays. Besides, the relationship between KAP-1 and DDX5 was verified by co-immunoprecipitation (Co-IP). The results showed that both of KAP-1 and DDX5 were upregulated in thyroid cancer cells. Loss-of-function experiments revealed that KAP-1 knockdown imparted suppressive effects on cell proliferation, migration and invasion, but promoted cell apoptosis. Additionally, KAP-1 was demonstrated to interact with DDX5 and positively regulate DDX5 expression. The following rescued experiments exhibited that the inhibitory effects of KAP-1 knockdown on cellular activities of thyroid cancer and Wnt/β-catenin signaling were also partly reversed by DDX5 overexpression. Moreover, activation of Wnt/β-catenin signaling retarded the anti-tumor activity of KAP-1 knockdown. In conclusion, the data in this study disclosed that KAP-1 silence helped to repress the cell proliferation, migration and invasion by degrading DDK5, so as to hinder the development of thyroid cancer.

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DMBT1 suppresses cell proliferation, migration and invasion in ovarian cancer and enhances sensitivity to cisplatin through galectin‐3/PI3k/Akt pathway

Cited by 11 publications

References 28 publications

METTL3‐mediated m6A modification of lnc RNA RHPN1‐AS1 enhances cisplatin resistance in ovarian cancer by activating PI3K/AKT pathway

METTL3‐mediated m6A modification of lnc RNA RHPN1‐AS1 enhances cisplatin resistance in ovarian cancer by activating PI3K/AKT pathway

Evaluation of CSTB and DMBT1 expression in saliva of gastric cancer patients and controls

Knockdown of KRAB domain-associated protein 1 suppresses the proliferation, migration and invasion of thyroid cancer cells by regulating P68/DEAD box protein 5

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