Antiproliferative effects of EGFR inhibitor Cetuximab and parp inhibitor combination on non-small cell lung cancer cell line A549 and cervical cancer cell line HeLa

Çeti̇n, İdi̇l; Topçul, Mehmet

doi:10.14715/cmb/2022.68.8.8

Cited by 6 publications

(4 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TRIM11, which has been linked to the migration and invasion of nasopharyngeal carcinoma, was found to be upregulated in NSCLC patients at both the mRNA and protein levels. Patients with high TRIM11 expression had lower survival rates 27 . Therefore, inhibiting TRIM11 may offer protection against NSCLC.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

Liang,

Li,

Zhang

et al. 2023

Clinical Respiratory J

View full text Add to dashboard Cite

Lung cancer is one of the leading causes of cancer‐related deaths worldwide, with non‐small cell lung cancer (NSCLC) being the most prevalent type. This study investigates the role of TRIM11 gene in NSCLC and its underlying mechanism. NSCLC patients were recruited from our hospital and showed upregulated TRIM11 mRNA and protein expressions. Patients with high TRIM11 expression had lower survival rates. TRIM11 gene was found to promote cell proliferation and reduce ROS‐induced ferroptosis in NSCLC. Additionally, TRIM11 gene induced AMPK expression and its regulation affected TRIM11's effects on cell proliferation and ferroptosis in NSCLC. IP analysis revealed that TRIM11 protein interacted with AMPK protein in NSCLC. These data confirmed that TRIM11 promotes cell proliferation and reduces ROS‐induced ferroptosis in NSCLC through AMPK. Hence, TRIM11 is a potential target for the treatment of NSCLC and other cancers.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Patients with high TRIM11 expression had lower survival rates. 27 Therefore, inhibiting TRIM11 may offer protection against NSCLC. Our study demonstrated that TRIM11 mRNA and protein expressions were upregulated in NSCLC patients.…”

Section: Discussionmentioning

confidence: 99%

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

Liang,

Li,

Zhang

et al. 2023

Clinical Respiratory J

View full text Add to dashboard Cite

show abstract

“…Accurately determined molecular features of non-small cell lung cancer are needed in order to investigate further therapeutic approaches. In recent years many scholars have studied its genetics and immunometabolism [2]. Among them, the study of RNA in cancer therapy has become an important research direction, and the relationship between covalent modification of RNA and cancer has become a new research field [3].…”

Section: Introductionmentioning

confidence: 99%

Expression patterns and prognostic role of m6A RNA methylation regulators in Non-small Cell Lung Cancer

Ming Zhang,

Congbo Yang,

Wen Dong

et al. 2024

Cell Mol Biol (Noisy-le-grand)

View full text Add to dashboard Cite

The purpose of this study was to investigate the expression pattern and prognostic role of m6A RNA methylation regulators in non-small cell lung cancer (NSCLC), we downloaded data from 422 patients from The Cancer Genome Atlas (TCGA) database. The relationship between the expression levels of m6A RNA methylation regulators and clinicopathological variables of NSCLC was analysed using R language. By analysing glioma data in TCGA, we found that a prognostic risk score model could be constructed based on 18 genes with m6A methylation modification. m6A gene alterations were significantly associated with tumour grade and tumour stage. Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression models were used to identify 2 m6A RNA methylation modifiers: IFG2BP2, and METTL14 to construct risk profiles. Based on the risk profile, patients were divided into high-risk and low-risk groups. The overall survival rate of the low-risk group was significantly higher than that of the high-risk group. The results suggest that the prognostic risk score model constructed by m6A methylation regulators can predict the prognosis of glioma patients. IFG2BP2 and METTL14 may be the key m6A methylation regulators involved in the development of NSCLC and can be used as the molecular markers for the prognosis of NSCLC.

show abstract

“…Among the diverse forms of this disease, non-small-cell lung cancer (NSCLC) stands out as the most prevalent but unfortunately carries a poor prognosis for patients [1]. One critical factor contributing to this unfavorable outlook is the insensitivity of NSCLC patients to conventional chemotherapeutic agents [2]. Their resistance to these treatments significantly limits the effectiveness of current interventions, underscoring the pressing need to identify novel and precise therapeutic targets.…”

Section: Introductionmentioning

confidence: 99%

The role of silymarin and MAPK pathway in the regulation of proliferation and invasion of non-small cell lung cancer cells

Jing Zhang,

Kaige Zhang,

Jing Li

et al. 2024

Cell Mol Biol (Noisy-le-grand)

View full text Add to dashboard Cite

We aimed to explore the role of silymarin and mitogen-activated protein kinase (MAPK) pathway in the regulation of proliferation and invasion of non-small cell lung cancer cells. Non-small cell lung cancer cells were cultured and divided into groups and treated with drugs, and A blank control group was set up. The concentration of silymarin in the experimental group was 10 mg/L, 20 mg/L and 40 mg/L, respectively, which were recorded as groups A, B and C, and three repeated experiments were performed in each group. Absorbance (A value), survival rate and number of invasions were measured at 490 nm 24 h and 48 h after treatment, and the protein expression levels of MMP-2, MMP-9, p-p38, p-JNK and p-ERK 1/2 of cells in each group were detected. There were differences in the A value (control group > Group A > Group B > Group C), cell survival rate (control group < group A < group B < group C) and the number of cell invasions (control group > Group A > Group B > group C) at 24 h and 48 h among all groups (P<0.05). After 24 h of administration, the mRNA expression of MMP-2 and MMP-9, P-P38 and P-JNK protein expression were significantly different among groups, and the control group was > group A > Group B > group C (P<0.05). There were no significant differences in protein expression levels of p38, JNK, ERK 1/2 and P-ERK 1/2 among all groups (P>0.05). Silymarin may inhibit the proliferation and invasion of non-small cell lung cancer cells by inhibiting the activity of MAPK pathway, and the higher the concentration, the more obvious the inhibition effect, which provides a basis for further research and treatment of non-small cell lung cancer.

show abstract

Antiproliferative effects of EGFR inhibitor Cetuximab and parp inhibitor combination on non-small cell lung cancer cell line A549 and cervical cancer cell line HeLa

Cited by 6 publications

References 29 publications

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

TRIM11 promotes cell proliferation of non‐small cell lung cancer through the inhibition of ferroptosis by AMPK

Expression patterns and prognostic role of m6A RNA methylation regulators in Non-small Cell Lung Cancer

The role of silymarin and MAPK pathway in the regulation of proliferation and invasion of non-small cell lung cancer cells

Contact Info

Product

Resources

About