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ANALISIS GEN KOMPARATIF KARSINOMA SEL SKUAMOSA PARU-PARU ANTARA INDIVIDU MEROKOK DAN TIDAK MEROKOK [Comparative Gene Analysis of Squamous Cell Lung Carcinoma Between Smoking and Non-smoking Individuals] Shemuel, Josia; Angelique, Priscilla; Josephine, Evalina; Ryan Fugaha, Daniel; Gabriela, Vania; Alhussain, Shaheer; Parikesit, Arli Aditya
Berita Biologi Vol 22 No 3 (2023): Berita Biologi
Publisher : BRIN Publishing (Penerbit BRIN)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.55981/beritabiologi.2023.908

Abstract

Squamous cell lung carcinoma (SCC) is a form of non-small cell lung cancer that commonly arises in the primary airway. The development of SCC is closely linked to changes in squamous cells that line the airways, primarily caused by exposure to tobacco smoke. To gain insights into SCC, bioinformatics techniques have been employed to detect biomarkers and analyze gene expression patterns, utilizing data from the Cancer Genome Atlas (TCGA) database, which was preprocessed for analysis. By employing DESeq2, a differential gene expression analysis method, identified genes showed significant variations in expression between smoking and non-smoking groups among the 11,530 genes examined. Notably, five genes, namely CT45A1, GCGR, TPTE, ABCC2, and PI16, were found to play a significant role in tumor development and were susceptible to under- or over-expression due to smoking. The majority of these genes were found to be underexpressed rather than overexpressed. These identified genes hold potential as biomarkers for tumor development and exhibit a strong correlation between smoking history and the development of SCC. However, a limitation encountered during this analysis was the unavailability of data from normal non-tumor patients, which could have facilitated a more comprehensive analysis of differential gene expression. Furthermore, this research gives a deeper implementation regarding the molecular mechanisms and genomics underlying SCC development, identifies differentially expressed genes associated with SCC and smoking history, and highlights potential biomarkers that warrant further investigation.
Phenotypic Plasticity and Functional Shift in Cisplatin-Resistant Cervical Cancer Cell Line Kristiani, Lidya; Ivana, Kathy; Gabriela, Vania; Rattu, Shereen Angelina; Tanoto, Joselyn Phoebe Wylma; Dearyza, Sonya; Angelica, Rosemarie; Wirabuana, Shareena; Dreesa, Amelia; Tehubijuluw, Marcella Diviani; Crystalia, Audrey Amira
Indonesian Journal of Cancer Vol 20, No 1 (2026): March
Publisher : http://dharmais.co.id/

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33371/ijoc.v20i1.1415

Abstract

Background: Cervical cancer remains the deadliest cancer among women. Furthermore, the development of resistance toward cisplatin, the golden standard treatment, has posed a significant challenge, threatening therapeutic efficacy and contributing to tumor recurrence. While enhanced DNA repair and drug inactivation have been implicated in resistance, their impact on cervical cancer remains poorly understood. This study aims to generate cisplatin-resistant cervical cancer cell lines to explore potential phenotypic and functional changes.Methods: We generated cisplatin-resistant cells through repeated exposure to increasing cisplatin concentrations up to 8 µM. Morphological changes were analysed using ImageJ software. Using manual hemocytometer counting, we generated a growth curve to assess cell growth, while a migration assay measured wound closure over time. Mitochondrial activity was evaluated using the MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay, and gene expression of p53, Bax, and β-actin was quantified via qPCR. Statistical analysis, including two-tailed Student’s t-tests, was performed to compare wild-type and treated groups, with significance at p 0.005. Graphs and data visualization were performed using Microsoft Excel and GraphPad Prism 10.2.3.Results: Cisplatin-resistant (CPR) HeLa cells exhibited concentration-dependent morphological changes, including multinucleated "giant cells" and neuron-like "transition cells" with extended arms, suggesting adaptive responses to cisplatin-induced stress. Cell size increased with higher cisplatin concentrations, potentially enhancing survival, while proliferation decreased, indicating an energy trade-off for resistance mechanisms. Mitochondrial activity declined in CPR cells, likely due to mitochondrial DNA damage, leading to reduced ATP production and oxidative stress. Gene expression analysis revealed decreased Bax levels, associated with reduced apoptosis. Despite these changes, migration capacity remained unchanged.Conclusions: The results reveal that cisplatin-resistant (CPR) HeLa cells develop distinct changes in characteristics, including morphologies and functional capacity, particularly decreased mitochondrial activity and proliferation in exchange for increased ability to avoid apoptosis. These findings deepen our understanding of cisplatin resistance and emphasize the need for innovative therapeutic strategies, such as targeting the altered characteristics and non-proliferative survival mechanisms of CPR cells.