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All Journal HAYATI Journal of Biosciences Microbiology Indonesia Health Science Journal of Indonesia Medical Journal of Indonesia Indonesian Journal of Cancer The Indonesian Biomedical Journal Universa Medicina Jurnal Farmasi Galenika (Galenika Journal of Pharmacy) Molecular and Cellular Biomedical Sciences (MCBS) Spektra: Jurnal Fisika dan Aplikasinya Acta Biochimica Indonesiana JFIOnline Majalah Kesehatan Pharmamedika The New Ropanasuri Journal of Surgery Narra J Indonesian Journal of Cancer Makara Journal of Science Jurnal Kedokteran Meditek Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education and Research Institute

Septelia I. Wanandi

Department Of Biochemistry And Molecular Biology, Faculty Of Medicine, Universitas Indonesia

Author-ID : 411928

Aerospace Engineering Agriculture, Biological Sciences & Forestry Biochemistry, Genetics & Molecular Biology Chemistry Dentistry Earth & Planetary Sciences Electrical & Electronics Engineering Energy Health Professions Immunology & microbiology Materials Science & Nanotechnology Medicine & Pharmacology Neuroscience Nursing Physics Public Health

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Regulation of Survivin Gene Expression in Stem Cell and Cancer Stem Cells and Emphasis Approach Nihayah, Silviatun; Wanandi, Septelia Inawati
Indonesian Journal of Cancer Vol 19, No 1 (2025): March
Publisher : http://dharmais.co.id/

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33371/ijoc.v19i1.1142

Background: Gene expression regulation is a method that cells utilize to enhance or decrease the output of specific genes (proteins or RNA). In biological and medical research such as cancer, gene expression is routinely observed. Survivin is a protein that is commonly produced in cancer cells and has the potential to be investigated. Survivin is a unique protein with two distinct roles: preventing apoptosis and regulating cell division. The inhibitory apoptosis protein (IAP) family includes the smallest member. Furthermore, Survivin is highly expressed in a variety of somatic stem cell types as well as human embryonic stem cells. Comparing most cancer cells to normal tissues, survivin is also present in higher amounts. This review aimed to examine the properties of survivin, how it is expressed in cancerous and normal stem cells, how it affects proliferation or apoptosis, and how to block their expression. Methods: The literature on the regulation of survivin expression in cancer cells and stem cells that was published in English between 2014 and 2024 is reviewed in this study. For articles, we looked through PubMed, Scopus, and the Google Scholar database. In order to support the theories, publications from before 2014 were also tracked down.Results: Molecular mechanism studies indicate that survivin participates in numerous signaling pathways, including MAPK, STAT3, b-catenin, Wnt, Notch, and others, and also controls the progression of the cell cycle and cytokinesis. Several elements, such as signaling pathway blockage siRNA technology, and CRISPR/Cas9 system have been discovered to aid in the induction of cancer cell death. Conclusion: Survivin is linked to several cancer survival-related pathways, contributing to carcinogenesis. Its expression is associated with treatment resistance, tumor development, and poor prognosis.

Roles of the Survivin BIR Domain in Cellular Apoptosis and Proliferation: An In Silico Study Nihayah, Silviatun; Wanandi, Septelia Inawati; Erlina, Linda; Syahrani, Resda Akhra
Makara Journal of Science Vol. 29, No. 1
Publisher : UI Scholars Hub

Show Abstract | Download Original | Original Source | Check in Google Scholar

Survivin is an antiapoptotic protein that is highly expressed in cancer cells. We investigated the dual roles of the Bacu-lovirus IAP Repeats (BIR) domain within survivin, encompassing both apoptosis and proliferation, through an in silico study. The protein-protein interaction (PPI) network of survivin was analyzed using Cytoscape software. Functional enrichment (FE) analysis and data from the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to identify the implicated signaling pathways. The binding affinity of the BIR domain with the targeted proteins was visualized via molecular docking analysis. Drawing insights from the PPI network and FE analysis, we identified two key proteins in-volved in apoptosis such as X-linked Inhibitor of Apoptosis Proteins (XIAP) and caspase-9, and proliferation such as Cyclin-dependent Kinase 1 (CDK1) and Inner Centromere Protein (INCENP) for further analysis of their binding with the survivin BIR domain. These proteins were found to bind to the BIR domain at the Thr34, Thr48, and Ser20 resi-dues that have critical roles to regulate the apoptosis and proliferation. This study provides future insights into how the BIR domain of survivin could emerge as a potential target for cancer treatment, such as determining knockout targets for the development of genome editing technology

Tumor apparent diffusion coefficient value and ratio in magnetic resonance imaging on cervical cancer Siregar, Trifonia Pingkan; Wanandi, Septelia Inawati; Darmiati, Sawitri; Kusuma, Fitriyadi; Sekarutami, Sri Mutya; Lisnawati; Prihartono, Joedo; Ilyas, Muhammad; Amalia, Ginva; Elfahmi, Khalida Ikhlasiya Tajdar Gefariena
Medical Journal of Indonesia Vol. 34 No. 2 (2025): June
Publisher : Faculty of Medicine Universitas Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.13181/mji.oa.257715

BACKGROUND Diffusion-weighted magnetic resonance imaging (DW-MRI) is a noninvasive, non-contrast sequence for cancer detection. Research involving DW-MRI in cervical cancer has revealed lower apparent diffusion coefficient (ADC) values. This study aimed to evaluate the difference in tumor ADC values and ADC ratios (tumor-to-urine and tumor-to-muscle) with respect to tumor staging (early versus late) and histopathology (squamous cell carcinoma versus adenocarcinoma). METHODS This retrospective study included 56 patients with cervical cancer, divided into early- and late-stage groups. DW-MRI was performed in all patients, and the tumor ADC value, ADC ratio between the tumor and urine (ADC ratiot−u), and ADC ratio between the tumor and gluteal muscle (ADC ratiot−m) were measured. Statistical methods were employed to assess the difference in the tumor ADC value, ADC ratiot−u, and ADC ratiot−m with respect to cervical cancer stages and histopathological findings. RESULTS The median tumor ADC value was lower in the early-stage group than in the late-stage cervical cancer (0.75 × 10−3 mm²/s versus 0.8 × 10−3 mm²/s, p = 0.022). However, no differences were observed in ADC ratiot−u and ADC ratiot−m concerning the tumor staging, nor in ADC value, ADC ratiot−u, and ADC ratiot−m concerning histopathological findings (p = 0.29, 0.67 and 0.35, respectively), with no significant differences in the ADC ratiot−u (p = 0.153) and ADC ratiot−m (p = 0.260). In receiver operating characteristic analysis, the tumor ADC value was 75.0% sensitive and 50.0% specific in predicting late-stage cervical cancer with a cut-off value of 0.750 × 10−3 mm2/s. CONCLUSIONS The median tumor ADC value in early-stage patients was significantly lower than in the late-stage patients, suggesting that tumor ADC value has valuable potential for characterizing cervical cancer staging.

Kurkumin Meningkatkan Sensitivitas Sel Kanker Payudara terhadap Tamoksifen Melalui Penghambatan Ekspresi P-glikoprotein dan Breast Cancer Resistance Protein: Curcumin Increased Breast Cancer Cells Sensitivity to Tamoxifen Through Inhibition of P-glycoprotein and Breast Cancer Resistance Protein Expressions Sianipar, Erlia Anggrainy; Louisa, Melva; Wanandi, Septelia Inawati
Jurnal Farmasi Galenika (Galenika Journal of Pharmacy) (e-Journal) Vol. 4 No. 1 (2018): (March 2018)
Publisher : Universitas Tadulako

The decreasing of sensitivity or resistance to tamoxifen occured after long-term treatment in breast cancer. One of the major factor in tamoxifen resistance is over expression of efflux transporter P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP). Curcumin has known as inhibitor of P-gp and BCRP. The addition of curcumin to the tamoxifen resistant cells is expected to increase the sensitivity of breast cancer cells to tamoxifen. This study aim to know the effect of curcumin in increasing the cell sensitivity to tamoxifen through inhibition of P-gp and BCRP transporter efflux. MCF-7 breast cancer cell line was induced with tamoxifen 1 ÂµM for 10 passage (MCF-7(T)), then cell viability and mRNA expression of P-gp and BCRP were analyzed. To the MCF-7(T) cells, curcumin was given at of 5/10/20 ÂµM with or without tamoxifen for 5 days and cell viability and mRNA expression of P-gp and BCRP were analyzed on day 5th. As positive control, verapamil 50 ÂµM was used as P-gp inhibitor, ritonavir 15 ÂµM and nelfinavir 15 ÂµM were used as BCRP inhibitor. The results showed that MCF-7(T) cells sensitivity to tamoxifen decreased with 11.8 times, the cell viability increased 10.82 fold and mRNA expression of P-gp and BCRP increased 4.04 fold. Then after administration of curcumin with or without tamoxifen for 5 days, the cell viability and the mRNA expression of P-gp and BCRP decreased. As conclusion, curcumin increased the sensitivity of MCF-7(T) to tamoxifen characterized by the decreasing of cell viability and mRNA expression of P-gp and BCRP. However, the administration of combination of curcumin with tamoxifen was more potent than just curcumin. The increased sensitivity was estimated at least partly through the inhibition of P-gp and BCRP mRNA expression by curcumin

FOXO1 and FYN Expression Trends in Breast Cancer Stem Cells: An Integrative Study of Single Nucleotide Polymorphism (SNP) Array and Quantitative PCR (qPCR) Analysis Ay Ly Margaret; Septelia Inawati Wanandi; Fadilah Fadilah; Rafika Indah Paramita
The Indonesian Biomedical Journal Vol 17, No 4 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i4.3656

BACKGROUND: Currently, identification of breast cancer stem cells (BCSCs) commonly relies on CD24-/CD44+ expression profiles. However, few studies have integrated genomic mutation data with experimental gene expression validation in CSC and non-CSC populations. Genotyping results of CD24-/CD44+ MDAMB-231 cells revealed 36 mutations in BCSCs compared to non-BCSCs, with upregulated FOXO1 and FYN that might represent promising candidate biomarkers for this subpopulation. Therefore, in this study, single nucleotide polymorphism (SNP) and quantitative polymerase chain reaction (qPCR) analysis were performed to assess the association between mutations and expression trends of FOXO1 and FYN in MDAMB-231 cell, as breast cancer cell model with stem-like traits and well-characterized profile.METHODS: Genomic DNA was isolated from BCSC and non-BCSC DNA from the MDAMB-231 cell line. Mutation analysis was conducted using PLINK, while gene expressions of FOXO1 and FYN were quantified by one-step SYBR Green-based qPCR, using 18s rRNA as a reference. Data was then analyzed with the Livak (2−∆∆Ct) method.RESULTS: Among 36 mutations found in BCSCs of the MDAMB-231 cell line, PTEN (rs786204914) and CHEK2 (rs587782401) were identified as pathogenic. While FOXO1 (2.989±2.817 vs. 1.072±0.388) and FYN (1.405±0.072 vs. 0.855±0.140) mRNA levels were found to be higher in CSCs compared to non-CSCs, though these differences was not statistically significant.CONCLUSION: Pathogenic mutations in CHEK2 and PTEN were detected within BCSC population, implying a potential influence on the expression of FOXO1 and FYN, though not statistically significant. These findings suggest a possible, but as yet unverified, association between gene mutations and expression patterns, emphasizing the importance of further functional studies to validate FOXO1 and FYN as biomarkers for BCSCs.KEYWORDS: breast cancer stem cells, FOXO1, FYN, PTEN, CHEK2, mutation, biomarker

Expression and Purification of Novel Peptide-Based Recombinant Proteins Targeting Breast Cancer Stem Cells Agusta, Istiqomah; Triwidyaningtyas, Silvia; Bela, Budiman; Mardiana, Mardiana; Wanandi, Septelia Inawati
Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education Research Institute Vol. 9 No. - (2025): Proceedings Book of International Conference and Exhibition on The Indonesian M
Publisher : Writing Center IMERI FMUI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.69951/proceedingsbookoficeonimeri.v9i-.327

Introduction: Peptides with specific affinity toward breast cancer stem cells (BCSCs), including GYSASRSTIPGK and GAIRIRLSEPLS, have gained interest in targeted cancer diagnostics; however, the low abundance of BCSCs often results in limited detection sensitivity. This study addresses this limitation by conjugating BCSC-specific peptides to self-assembling Human Papillomavirus (HPV16) L1 protein, resulting in virus-like particles composed of 72 pentamers that provide substantial signal amplification. In addition, the SpyTag–SpyCatcher system derived from the Streptococcus pyogenes CnaB2 domain provides a robust strategy to enhance peptide–protein stability. Objectives: This study aimed to express and purify three recombinant proteins as key components for assembling a BCSC-specific diagnostic construct: HPV16 L1–SpyTag, SpyCatcher–GYSASRSTIPGK, and SpyCatcher–GAIRIRLSEPLS. Methods: Recombinant genes encoding the target proteins were expressed in Escherichia coli (E. coli) BL21(DE3) following IPTG induction for 1–4 hours. Bacterial cells were harvested and lysed under native or denaturing conditions, and recombinant proteins were purified using Ni-NTA affinity chromatography. Results: SDS–PAGE analysis showed clear bands at the expected molecular weights for HPV16 L1–SpyTag (58.5 kDa), SpyCatcher–GYSASRSTIPGK, and SpyCatcher–GAIRIRLSEPLS (~15 kDa), with induction-dependent increases in band intensity. The SpyCatcher–peptide fusions were predominantly soluble and purified under native conditions, whereas HPV16 L1–SpyTag was largely insoluble and required denaturing purification. Conclusion: HPV16 L1–SpyTag and SpyCatcher–peptide fusions were successfully expressed and purified in E. coli, establishing a versatile platform with potential to enhance BCSC-targeted detection and treatment strategies in breast cancer.

Temozolomide Resistance is Associated with Upregulated MICB mRNA Expression and Protein Secretion in Human Glioblastoma Cells Kevin Johanes Kawengian; Septelia Inawati Wanandi; Febriana Catur Iswanti; Remizar Alpaddli
The Indonesian Biomedical Journal Vol 18, No 3 (2026)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v18i3.4250

BACKGROUND: Standard treatment for glioblastoma multiforme (GBM) chemotherapy with temozolomide (TMZ) is often limited by chemoresistance, which is correlated with cancer immune evasion caused by the dysregulation of natural killer group 2 member D ligands (NKG2DL). While suppression of NKG2DL facilitates cancer progression, how chemoresistance regulates NKG2DL expression remains unclear. This study was conducted to examine the association of TMZ resistance with the expression and secretion of the NKG2DL subtype, MHC class I chain-related protein B (MICB), in human GBM cells.METHODS: An experimental in vitro study was conducted using TMZ-sensitive (U87MG) and intrinsically TMZ-resistant (T98G) human GBM cell lines. MICB mRNA expression was analyzed via quantitative reverse transcription polymerase chain reaction (qRT-PCR). Surface protein expression and extracellular secretion of MICB were measured using flowcytometry and enzyme-linked immunosorbent assay (ELISA), respectively.RESULTS: Repeated TMZ exposure successfully induced resistance in U87MG-R (+TMZ) cells, yielding significantly higher cell viability (p<0.01) and slower proliferation rates compared to parental U87MG cells. Following 2-days TMZ treatment, both intrinsically resistant T98G and adaptively resistant U87MG-R (+TMZ) cells, demonstrated a significant increase in MICB mRNA levels (p<0.05 and p<0.0001, respectively) and extracellular secretion of soluble MICB protein (p<0.01 and p<0.01, respectively), compared to TMZ-sensitive counterparts. Conversely, MICB surface protein level after 2-days TMZ treatment was significantly reduced in both T98G (p<0.0001) and U87MG-R (+TMZ) (p<0.01) cells relative to the respective U87MG cells.CONCLUSION: GBM cell resistance to TMZ was associated with an upregulation of MICB mRNA transcription and extracellular protein secretion, and concurrently with a suppression of MICB expression on the cell surface. These conditions may lead to a cellular adaptive mechanism to develop resistance to TMZ and may represent a strategic route to evade native host immune. KEYWORDS: glioblastoma multiforme, temozolomide, cancer chemoresistance, MHC class I chain-related protein B (MICB), natural killer group 2D receptor (NKG2D)

Targeting tumor associated macrophages to alternate cancer stem cells and tumor microenvironment milieu Mahdaleny Mahdaleny; Septelia Inawati Wanandi; Noorwati Sutandyo; Febriana Catur Iswanti
Universa Medicina Vol. 45 No. 2 (2026)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2026.v45.310-321

Macrophages in the tumor microenvironment are involved in promoting cancer growth and enabling it to evade therapies. By acting as something like a tumor's "underground," these cells dampen down the "calls for help" that chemotherapy or radiotherapy might otherwise trigger. They also appear to enable some cells in the cancers to reset themselves into cancer stem cells (CSCs), allowing them to divide and differentiate. Cancer stem cells are compelled to initiate tumors and maintain their growth. In part, the tumor-associated macrophages (TAMs) effect this by secreting cytokines with well-established roles in regulating stemness, as well as proteins that govern cell migration and are known to help keep CSCs in the niche where the tumor formed and maintain the tumor. Prognostic studies have found that TAMs are associated with worse patient outcomes. This article reviews the existing knowledge on TAMs in supporting the survival and maintenance of CSCs, increasing tumor resilience and resistance to therapy. We did a systematic review using the keywords CSC, TAM, tumor microenvironment (TME), and extracellular matrix remodeling from the following databases: ScienceDirect, PubMed, NCBI, Nature, Google Scholar, and Oxford Academic for articles published between 2010 to 2026. The underlying premise of the current investigation is that macrophages facilitate the maintenance of the "stemness" characteristics of CSCs. The TAM-CSC alliance must be interrupted to improve therapeutic outcomes and reduce tumor recurrence. Our review focuses on addressing the difficulties presented by CSCs and TME through advanced research techniques and specific combination treatments. This alternative method offers a less harsh and more effective therapy that will improve the patient’s outcomes by effectively eradicating tumor cells and modifying the tumor microenvironment to enhance the immune system's capability to combat the tumor.

Co-Authors . ANDI Abdul Halim Sadikin Adang Bachtiar Agnes Kurniawan Agusta, Istiqomah Alice Tamara Amalia, Ginva Amarila Malik Andi A. Victor ANDI YEHUDA ANDREW ROBERT COSSINS Ani R. Prijanti Ani Retno Prijanti Anto Sulaksono Asmarinah Ay Ly Margaret Ay Ly Margareth Ayu Suraduhita Bagus Ramasha Amangku Bethy S. Hernowo Budiman Bela CENMI MULYANTO Chatarina Umbul Wahyuni Daniel Marcellius Simadibrata Darmiati, Sawitri DARYL ROBERT WILLIAMS Dewi Muliaty Dewi Sumaryani Soemarko Dewi, Yulia Ratna Dimas Priantono Din Syafruddin Dwi Retna Lestari Elfahmi, Khalida Ikhlasiya Tajdar Gefariena Elisna Syahruddin Elvira Hinsch Elvira Yunita Erlia Anggrainy Sianipar Erlina, Linda Eziefule, Oluebube Magnificient Fadilah Fadilah Febriana C. Iswanti Febriana Catur Iswanti FERY ARDIANSYAH Fitriyadi Kusuma Franciscus D. Suyatna Frans Ferdinal Ghanny, Niken Rahmah H. J. Freisleben Habibah Muhiddin HANS-JOACHIM FREISLEBEN HANS-JOACHIM FREISLEBEN HANS-JOACHIM FREISLEBEN Harahap, Alida R. HARALD HUBER HARALD HUBER Hendrik Kurniawan Herbowo A. Soetomenggolo Ida Gunawan IMAN SANTOSO IMAN SANTOSO Irawan Yusuf Irene Dian JÃƒÂ¶rg Gromoll Jeanne A. Pawitan Joedo Prihartono Karina Teja Putri Kartolo, Wiwi A. Kawengian, Kevin Johanes Kevin Johanes Kawengian Lisnawati Mahdaleny Mahdaleny Mardiana Mardiana Maria Dara Novi Handayani, Maria Dara Novi Maria Maghdalena Melva Louisa MICHAEL THOMM Mizuno, Seiya Mohamad Sadikin Muchlis Ramli Muchtaruddin Mansyur Muhammad Arif Muhammad I. Saleh Muhammad Ilyas Mukharjon Mukharjon Murdani Abdullah Nabillah, Deya Adiby Nafrialdi Nafrialdi Nihayah, Silviatun Noorwati Sutandyo Noorwati Sutandyo Novi S. Hardiany Novi Silvia Hardiany Noza Hilbertina Nukman H. Moeloek Nukman Moeloek Nurjati C. Siregar Nurjati Chairani Siregar Paramita, Rafika I. Paramita, Rafika Indah Parwati Abadi Soekarno Puji B.S. Asih Purnamawati Purnamawati Purnomo Soeharso Puspita E. Wuyung Puspita Eka Wuyung Putri, Putu Indah Paramita Adi Raafqi Ranasasmita Radiana D. Antarianto Remizar Alpaddli Reni Paramita Resda Akhra Syahrani Resda Akhra Syahrani Rianto Setiabudy Rini Puspitaningrum Rini Puspitaningtum RONDANG ROEMIATI SOEGIANTO RONDANG ROEMIATI SOEGIANTO RONDANG ROEMIATI SOEGIANTO Rosari Saleh Rostika Flora Sari, Dewi H. Sarwono Waspadji Sekar Arumsari SEKAR ARUMSARI, SEKAR Sekarutami, Sri Mutya SERUNI K.U. FREISLEBEN SERUNI KUSUMA UDYANINGSIH FREISLEBEN Sianipar, Erlia Anggrainy Siregar, Nurjati Siufui Hendrawan Sonar Panigoro SRI HANDAYANI Sri S. Ningsih, Sri S. Sri S. Sudardjat Sri W. Dwintasari Sri W.A. Jusman Sri Widia A.Jusman Syahrani, Resda A. Syahrani, Resda Akhra Syaiful Ichwan Syarifah Dewi Syarifah Salma Tjahjono D. Gondhowiardjo Trifonia Pingkan Triwidyaningtyas, Silvia Vanny Narita Wahyuning Ramelan Warsito Purwo Taruno Watanabe, Yukihide Wawaimuli Arozal Wawan Mulyawan Wawan Mulyawan Wibisana, I GNG. Yalista Fatia Nadia Yefta Moenadjat Yohana Yohana Yohanna Sorontou Yuni Ahda Yurika Sandra ZESSINDA LUTHFA ZESSINDA LUTHFA

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