Association of the OPRM1 variant rs1799971 (A118G) and clinical manifestations in tramadol poisoned patients: a cross-sectional study.

INTRODUCTION: The opioid receptor mu1 is a protein coding gene that can have different codes for a protein and may have variations (polymorphisms) affecting how opioids work. The aim of this study was to investigate the prevalence of the most common opioid receptor mu1 polymorphism (A118G) and any relationship between this polymorphism and features following tramadol overdose. MATERIALS AND METHODS: This was a cross-sectional study of patients admitted with tramadol poisoning to an Iranian hospital. These patients were not taking any other drugs or medications and had no history of seizures. RESULTS: The results showed that among the 83 patients included in the study, 57 (69 per cent) had the AA genotype, 25 (30 per cent) had the AG genotype, and one (1 per cent) had the GG genotype for the opioid receptor mu1 A118G polymorphism. Nausea and/or vomiting occurred in nine (11 per cent) patients and dizziness in 38 (46 per cent) patients. Serious adverse events included seizures in 51 (60 per cent) patients and respiratory failure requiring mechanical ventilation in 21 (25 per cent) patients. However, there was no significant association between the opioid receptor mu1 A118G polymorphism and these adverse events. DISCUSSION: In our study, the frequency of the A allele was greater than the G allele, and the AA genotype was more prevalent than AG. The GG genotype was the least common among the polymorphisms of opioid receptor mu1 rs1799971. There was no significant association between the opioid receptor mu1 A118G polymorphism and symptoms in tramadol-poisoned patients. Although these allele proportions are similar to the results reported in other Caucasian populations, they are dissimilar to the findings in Chinese and Singaporean populations. In these Asian studies, the predominant allele was the G allele. It has been suggested that a mutated G allele will decrease the production of opioid receptor mu1-related messenger ribonucleic acid and related proteins, leading to fewer mu-opioid receptors in the brain. CONCLUSIONS: This study found no significant association between the opioid receptor mu1 A118G polymorphism and adverse outcomes in tramadol-poisoned patients. However, more research is needed to draw more definitive conclusions due to the limited evidence and variability of opioid receptor mu1 polymorphisms in different populations.

Correlation of IDH1 gene expression error in breast tumor biopsy in patients with invasive ductal carcinoma.

One of the most important cancers in terms of worldwide prevalence is breast tumors, which have been less investigated in correlation with the enzyme Isocitrate Dehydrogenase 1 (IDH1) gene. The aim of this study was that expression of this gene could have significant effects on the progression of metastasis and invasive disease in breast cancer patients. We used the molecular method of RT-PCR with SYBR-Green to analyze breast tumor tissue from patients with metastasis and non-metastasis, the latter confirmed by the pathology department of Shohada-e Tajrish Hospital (serving as a control group). Also, patients population and its relationship with the degree of tumor in the IDH1 gene was investigated. The IDH1 gene has shown high expression in patients with metastatic breast cancer rather than in patients with non-metastatic breast cancer. The metastatic samples were compared with non-metastatic samples for IDH1 mRNA expression. In this research work, 72.5% (29 samples) were up-regulated in comparison to 27.5% of samples (11 samples) that did not exhibit high expression (P=0.000).  This study examined the IDH1 gene expression, suggesting that changes in this gene's expression could impact the prognosis of breast cancer. However, further research is needed to draw definitive conclusions.

Oncolytic viruses in lung cancer treatment: a review article.

Lung cancer has a high morbidity rate worldwide due to its resistance to therapy. So new treatment options are needed to improve the outcomes of lung cancer treatment. This study aimed to evaluate the effectiveness of oncolytic viruses (OVs) as a new type of cancer treatment. In this study, 158 articles from PubMed and Scopus from 1994 to 2022 were reviewed on the effectiveness of OVs in the treatment of lung cancer. The oncolytic properties of eight categories of OVs and their interactions with treatment options were investigated. OVs can be applied as a promising immunotherapy option, as they are reproduced selectively in different types of cancer cells, cause tumor cell lysis and trigger efficient immune responses.

A lot of research has been done to find a cure for lung cancer. Among the methods investigated is the treatment of cancer using a type of virus called an oncolytic virus (OV). Since tumors have unique properties, OVs tend to bind to them and activate immune cells to kill them. This article reviews the combination of OVs with other common cancer treatments which improves their effectiveness, causes fewer reactions and brings better results.

Microbiome modulation in inflammatory diseases: Progress to microbiome genetic engineering.

Recent developments in sequencing technology and analytical approaches have allowed researchers to show that the healthy gut microbiome is very varied and capable of performing a wide range of tasks. The importance of gut microbiota in controlling immunological, neurological, and endocrine function is becoming well-recognized. Thereby, numerous inflammatory diseases, including those that impact the gastrointestinal system, as well as less obvious ones, including Rheumatoid arthritis (RA), cancer, gestational diabetes (GD), type 1 diabetes (T1D), and type 2 diabetes (T2D), have been linked to dysbiotic gut microbiota. Microbiome engineering is a rapidly evolving frontier for solutions to improve human health. Microbiome engineering seeks to improve the function of an ecosystem by manipulating the composition of microbes. Thereby, generating potential therapies against metabolic, inflammatory, and immunological diseases will be possible through microbiome engineering. This essay first provides an overview of the traditional technological instruments that might be used for microbiome engineering, such as Fecal Microbiota Transplantation (FMT), prebiotics, and probiotics. Moreover, we will also discuss experimental genetic methods such as Metagenomic Alteration of Gut microbiome by In situ Conjugation (MAGIC), Bacteriophage, and Conjugative plasmids in manipulating intestinal microbiota.

Non-coding RNAs: A new frontier in benzene-mediated toxicity.

One of the most frequent environmental contaminants, benzene is still widely used as an industrial solvent around the world, especially in developing nations, posing a serious occupational risk. While the processes behind the toxicity of benzene grounds are not fully understood, it is generally accepted that its metabolism, which involves one or more reactive metabolites, is crucial to its toxicity. In order to evaluate the many ways that benzene could influence gene regulation and thus have an impact on human health, new methodologies have been created. The pathophysiology of the disorder may result from epigenetic reprogramming caused by exposure to benzene, including changes in non-coding RNA (ncRNA) markers, according to recent studies. We are interested in the identification of hazardous regulatory ncRNAs, the identification of these ncRNAs' targets, and the comprehension of the significance of these interactions in the mechanisms behind benzene toxicity. Hence, the focus of recent research is on long non-coding RNAs (lncRNAs), circular RNAs (circRNAs) and microRNAs (miRNAs), and some of the more pertinent articles are also discussed.

Clinical and genetic characterization of neuronal ceroid lipofuscinoses (NCLs) in 29 Iranian patients: identification of 11 novel mutations.

Neuronal ceroid lipofuscinoses (NCLs) are neurodegenerative lysosomal storage diseases which are considered among the most frequent causes of dementia in childhood worldwide This study aimed to identify the gene variants, molecular etiologies, and clinical features in 23 unrelated Iranian families with NCL. In total, 29 patients with neuronal ceroid lipofuscinoses (NCLs), diagnosed based on clinical manifestations, MRI neuroimaging, and electroencephalography (EEG), were recruited for this study. Through whole-exome sequencing (WES), functional prediction, Sanger sequencing, and segregation analysis, we found that 12 patients (41.3%) with mutations in the CLN6 gene, 7 patients (24%) with the TPP1 (CLN2) gene variants, and 4 patients (13.7%) with mutations in the MFSD8 (CLN7) gene. Also, mutations in each of the CLN3 and CLN5 genes were detected in 2 cases and mutations of each PPT1 (CLN1) and CLN8 gene were observed in only 1 separate patient. We identified 18 different mutations, 11 (61%) of which are novel, never have been reported before, and the others have been previously described. The gene variants identified in this study expand the number of published clinical cases and the variant frequency spectrum of the neuronal ceroid lipofuscinoses (NCLs) genes; moreover, the identification of these variants supplies foundational clues for future NCL diagnosis and therapy.

Non-coding RNAs: An emerging player in particulate matter 2.5-mediated toxicity.

Exposure to air pollution has been connected to around seven million early deaths annually and also contributing to higher than 3 % of disability-adjusted lost life years. Particulate matters (PM) are among the key pollutants that directly discharged or formed due to atmospheric chemical interactions. Among these matters, due of its large surface area, PM2.5 may absorb a different harmful and toxic substances. One of the outcomes of such environmental disturbance is oxidative stress which affects cellular processes including apoptosis, inflammation, and epithelial mesenchymal transition. Non-coding RNAs (ncRNA) such as, miRNAs, lncRNAs, and circRNAs are classified as non-protein coding RNA's. Over the past few years these small molecules have been gaining so much attention since they participate in variety of physiological and pathological processes and their expression change during disease periods. Regarding epigenetic properties, ncRNAs play an important function in organism's response to environmental stimulus. In this manner, it was revealed that exposure to PM2.5 may cause epigenetic reprogramming, such as, ncRNAs signature's alteration, which can be effective concerning pathophysiology state. In this review, we describe PM2.5 impact on ncRNAs and excavate its roles in toxicity caused by PM2.5.

siRNA and targeted delivery systems in breast cancer therapy.

Recently, nucleic acid drugs have been considered as promising candidates in treatment of various diseases, especially cancer. Because of developing resistance to conventional chemotherapy, use of genetic tools in cancer therapy appears inevitable. siRNA is a RNAi tool with capacity of suppressing target gene. Owing to overexpression of oncogenic factors in cancer, siRNA can be used for suppressing those pathways. This review emphasizes the function of siRNA in treatment of breast tumor. The anti-apoptotic-related genes including Bcl-2, Bcl-xL and survivin can be down-regulated by siRNA in triggering cell death in breast cancer. STAT3, STAT8, Notch1, E2F3 and NF-κB are among the factors with overexpression in breast cancer that their silencing by siRNA paves the way for impairing tumor proliferation and invasion. The oncogenic mechanisms in drug resistance development in breast tumor such as lncRNAs can be suppressed by siRNA. Furthermore, siRNA reducing P-gp activity can increase drug internalization in tumor cells. Because of siRNA degradation at bloodstream and low accumulation at tumor site, nanoplatforms have been employed for siRNA delivery to suppress breast tumor progression via improving siRNA efficacy in gene silencing. Development of biocompatible and efficient nanostructures for siRNA delivery can make milestone progress in alleviation of breast cancer patients.

Bcl-2 expression in cell lines breast cancer and death program.

Breast cancer is a hormone-dependence and heterogenic disease. Drug resistance is the main reason for the failure of breast cancer treatment. Combinatory medications are methods for treatment but they are not sufficient in action. However, new approaches like molecular therapy reveal a new insight into cancer treatment. Studies show that Bcl-2 gene family inhibitors and ER blockers cause the improvement of recovery. Interfering molecules such as antisense ones can inhibit the expression of Bcl-2 and push the cancer cells to apoptosis. Our team designed a new Antisense Oligonucleotide (ASO) based on Antisense oligo G3139. MCF-7 and MDA-MB-231 cell lines were used to evaluate cellular proliferation. Liposomes and cationic nano-complex (Niosome) are used to increase the cellular delivery of ASO and Tamoxifen. We also investigated the cytotoxicity and apoptotic effects of Tamoxifen, naked ASO and Nano-packed ASO. The results indicated significant down-regulation of the Bcl-2 gene and inhibition of MCF-7 and MDA-MB-231 cellular proliferation. Flow-cytometry showed early apoptosis in all cell groups. The newly designed ASO reduced the expression of the Bcl-2 gene. It also had a synergistic effect with the Tamoxifen. The cationic nano-complex (Niosome) was more efficient than the liposome in delivering designed oligo antisense Bcl-2 in the cancer cells.

Molecular Characteristics of TYK2 Gene Expressions in Patients with Colorectal Cancer.

Background: TYK2 is a member of the JAK family and is known to mediate signals of multiple cytokines that play a crucial role in immune and inflammatory signaling. Activation of TYK2 in tumor cells has been linked to promote cell survival, growth, and invasion. This study aimed to investigate the expression of tyrosine kinase 2 (TYK2) in colorectal cancer (CRC) and adjacent control tissues. Materials and Methods: Quantitative Real-Time PCR (qRT-PCR) method was elaborated to examine the expression levels of TYK2 in 100 colorectal tumor tissues and adjacent tissues as a control. Furthermore, we analyzed the diagnostic power of the mentioned TYK2 by plotting the receiver operating characteristic (ROC) curve. Results: Our results revealed that the expression level of TYK2 was significantly up-regulated in CRC patients sample compared to the adjacent sample of the control group. Analysis of patient's clinic pathological features shows that expressions TYK2 were differently associated with lymph vascular invasion and TMN stage (P < 0.0001, P < 0.0006). Conclusion: These results indicated that TYK2 levels potential biomarkers for diagnosing colorectal cancer may be identified.

The T Cell Receptor Repertoire Diversity Following Hematopoietic Stem Cell Transplantation.

Immune reconstitution after hematopoietic stem cell transplantation (HSCT) with a conditioning regimen has appeared to be a promising treatment for autoimmune diseases and hematologic malignancies. This study aimed to assess the T cell receptor (TCR) repertoire diversity in CD4+ cells of patients with hematological malignancies who received allogeneic or autologous HSCT. The diversity of the TCR repertoire was evaluated in 13 patients with hematologic malignancies before and four months after HSCT. Amino acid changes in the 25 Vß families were evaluated using Spectratyping and data were presented as Hamming distance (HD). HD more than 20% was considered a change in TCR repertoire after HSCT. The mean HD was significantly changed after transplantation in all Vß gene families, with most amino acid changes in p4 and p22 families. There was a strong negative correlation between the HD as the index of TCR repertoire and age (r = -0.62,). The results revealed no association between HD mean and parameters such as sex, disease, conditioning regimen, and type of transplantation. Our data revealed that commonly used conditioning regimens in Iran could successfully cause TCR repertoire diversity in patients with hematologic malignancies in the short term. The amount of change in TCR repertoire was inversely correlated with the increasing age of patients.

An in silico comparative transcriptome analysis identifying hub lncRNAs and mRNAs in brain metastatic small cell lung cancer (SCLC).

Small cell lung cancer (SCLC) is a particularly lethal subtype of lung cancer. Metastatic lung tumours lead to most deaths from lung cancer. Predicting and preventing tumour metastasis is crucially essential for patient survivability. Hence, in the current study, we focused on a comprehensive analysis of lung cancer patients' differentially expressed genes (DEGs) on brain metastasis cell lines. DEGs are analysed through KEGG and GO databases for the most critical biological processes and pathways for enriched DEGs. Additionally, we performed protein-protein interaction (PPI), GeneMANIA, and Kaplan-Meier survival analyses on our DEGs. This article focused on mRNA and lncRNA DEGs for LC patients with brain metastasis and underlying molecular mechanisms. The expression data was gathered from the Gene Expression Omnibus database (GSE161968). We demonstrate that 30 distinct genes are up-expressed in brain metastatic SCLC patients, and 31 genes are down-expressed. All our analyses show that these genes are involved in metastatic SCLC. PPI analysis revealed two hub genes (CAT and APP). The results of this article present three lncRNAs, Including XLOC_l2_000941, LOC100507481, and XLOC_l2_007062, also notable mRNAs, have a close relation with brain metastasis in lung cancer and may have a role in the epithelial-mesenchymal transition (EMT) in tumour cells.

Progress toward molecular therapy for diabetes mellitus: A focus on targeting inflammatory factors.

Diabetes mellitus (DM) has been the most prevalent global metabolic disease, turning into a serious risk for human health. Several researches have recorded a role for inflammation and immunity in the pathogenesis of both in T1DM and in T2DM. Lots of chemical agents are available to control and to cure diabetic patients, which are not always sufficient for euglycemia maintenance and late stage diabetic complications avoidance. Therefore, newborn therapeutic methods to refine clinical outcomes in DM are required. Nucleic-acid-based therapy also known as gene expression level regulator within the target cells has been calculated to be promising in various diseases. Thus, pronounced attempts have been dedicated to develop new targeted molecular therapy aimed at improving insulin resistance in DM. This review mainly focuses on recent progress in DM molecular therapy and whether, has potential efficacy against inflammatory mediators involved in DM.

Leu226Trp CACNA1A variant associated with juvenile myoclonic epilepsy with and without intellectual disability.

OBJECTIVE: Epilepsy is a disease of Central Nervous System (CNS) characterized by abnormal brain activity and recurrent seizures and is considered a clinically and genetically heterogeneous disease. Here, we investigated pathogenic genetic alteration and described the clinical characteristics of three Iranian family members affected by Idiopathic Generalized Epilepsy (IGE) with and without intellectual disability. METHODS: A non-consanguineous Iranian family with juvenile myoclonic epilepsy was enrolled in the study. The comprehensive neurological evaluation included motor and sensory skills, vision, hearing, speech, coordination, and mood. Whole-exome Sequencing (WES) was performed on the proband to detect probable pathogenic variant, and after the filtering process, probable variants were evaluated with familial segregation analysis using Sanger sequencing. RESULTS: Using WES, we identified a heterozygous missense substitution (NM_023035.3:c.T677G:p.Leu226Trp) in CACNA1A gene in the studied family with juvenile myoclonic epilepsy with and without intellectual disability and psychiatric phenotype. Considering the patients' clinical synopsis, familial segregation analysis, and literature review, we postulated this variant to be causative of the disease. Indeed, the resulting missense mutation of Leu226Trp affects a highly conserved residue supporting our hypothesis that this mutation is potentially pathogenic. CONCLUSION: To the best of our knowledge, this is the first report of juvenile myoclonic epilepsy related to CACNA1A gene. Our results provide evidence for expanding the clinical and molecular findings related to the CACNA1A gene.

Evaluation of the current MicroRNAs expression levels as potential biomarkers in Oral Squamous Cell Carcinoma.

As the most common malignancy, oral squamous cell carcinoma (OSCC) is typically fatal. The survival of patients with oral cancer has not improved, and tumor recurrence remains high. During tumorigenesis, microRNAs (miRNAs) regulate gene expression. Patients' life expectancy can be determined by prognostic survival biomarkers, which can focus therapy on specific targets. This study evaluated five miRNAs associated with OSCC for their prognostic impact. It was determined through microarray analysis and quantitative reverse transcription polymerase chain reaction that there was a significant difference in the expression of miRNAs between OSCC patients and control patients in plasma. We used the unpaired t-tests and the Mann-Whitney test to conduct the statistical analysis. Based on the study's results, five miRNAs have been found to have significantly different expression levels in the plasma of patients with OSCC; in particular, miR-31 was found to have a significantly higher expression level in OSCC patients' plasma as compared with healthy controls. Aside from that, there was a significant reduction in the expression of miR-100, miR-199a, miR-203, and mir345 in the plasma of OSCC patients (P < 0.05). To better understand the importance of miRNAs in OSCC, various OSCC cases were analyzed. Detecting miRNAs in plasma may be a useful diagnostic tool for oral squamous cell carcinoma.

Evaluation of Hepatoprotective and Gastroprotective Activities of Paspalidium flavidum Leaves Extract in Experimental Animal Models.

Paspalidium flavidum (watercrown grass), a medicinal plant, is traditionally used in liver ailments and stomach problems. The hepatoprotective and gastroprotective activities of the aqueous methanol extract of Paspalidium flavidum (AMEPF) were studied in experimental animal models. Paracetamol and aspirin were used to induce hepatotoxicity and gastric ulcer in rats, respectively. Biochemical hepatic parameters, gastric pH, total acidity, ulcer index, percentage protection, nitric oxide and TNF-α were measured in AMEPF-treated groups. Moreover, GC-MS analysis of AMEPF was performed. Pretreatment with AMEPF improved the blood lipid profile and restored liver function tests in paracetamol-induced hepatotoxicity. While in aspirin-induced gastric ulcer, oral administration of AMEPF significantly reduced (P<0.05) the gastric lesions, total acidity and ulcer scoring index, TNF-α with upregulation of nitric oxide when compared with the Diseased group. AMEPF exhibited anti-lipid peroxidation activity. Histopathological studies were in good agreement with the biochemical findings. GC-MS analysis revealed the presence of anti-oxidant phyto-constituents, including oleic acid and 1,2-benzenedicarboxylic acid, mono(2-ethylhexyl) in AMEPF. This study suggested that aqueous methanol extract from the leaves of P. flavidum has beneficial hepatoprotective and gastroprotective activities related to its anti-oxidant phytochemicals.

Diagnostic of Cytokeratin-19 Gene Expression in Iranian Breast Cancer Patients.

Sentinel lymph node (SLN) biopsy is currently the recommended procedure for axillary staging in clinically node-negative early breast cancer at diagnosis. The present study aimed to identify Cytokeratin-19 (CK19) gene profiles that accurately predicted the outcome of breast cancer patients. Fifty tumor samples from breast cancer patients were analyzed for the expression of the CK19 gene using quantitative PCR. Also, normal breast tissues (N = 50) were taken from the same patients that had undergone partial or total mastectomy. This gene signature was confirmed based on tumor's stage, grade, and estrogen receptor (ER) status, using conditional logistic regression. Based on these findings, the negative reported lymph nodes for metastasis had micrometastasis in significant values. There was a significant difference between normal and cancer samples in  CK19 expression. In this sentinel node evaluation, the relationship of this gene with tumor characteristics needs to be established and discussed finding a clear role for this gene in tumor outcome.

Clinical and molecular spectrum of P/Q type calcium channel Cav2.1 in epileptic patients.

BACKGROUND: Epilepsy is a neurological disorder characterized by the potential to induce seizure and accompanied by cognitive, psychological, and social consequences. CACNA1A gene is a voltage-gated P/Q-type Cav2.1 channel that is broadly expressed in the central nervous system, and the pathogenic variants within this gene may be associated with the epileptic phenotype. In the present study, we collected clinical and molecular data related to epileptic patients with CACNA1A pathogenic variants and investigated possible meaningful relationship between age at onset, neurodevelopmental disorders, type of seizures, brain imaging abnormalities, genotype, and protein domains. RESULTS: In our retrospective literature studies, from among 890 articles reviewed, a total of 90 individuals were related to epilepsy phenotype. Our findings showed that about 90 percent of patients have shown the first symptoms in childhood and teenage years and different types of neurodevelopmental disorders, such as intellectual disability, developmental arrest, and behavioral disorders, have been common findings for these patients. Further, a wide range of abnormalities have been observed in their brain imaging, and generalized seizures have been the most type of seizures in these patients. However, our data showed no specific genotype-phenotype correlation in epileptic patients with CACNA1A pathogenic alterations. CONCLUSIONS: Our study focused on epileptic phenotype in patients with CACNA1A pathogenic variants and showed a wide range of clinical and molecular heterogeneity with no specific genotype-phenotype correlation. It seems that incomplete penetrance, de-novo variants, and modifier genes are obstacles in predicting the clinical outcome.

Altered expression of STAT genes in periodontitis.

Signal Transducer and Activator of Transcription (STAT) pathway is functionally located downstream of Janus kinases proteins and can integrate signals from diverse pathways, thus regulating several aspects of immune responses. Although contribution of STAT proteins in the pathogenesis of several inflammatory conditions has been confirmed, their role in the development of periodontitis has been less appraised. Thus, we assessed levels of STAT transcripts in the periodontal tissues and circulation of affected individuals compared with the corresponding controls. Expression of STAT1 was remarkably lower in tissues samples of patients compared with control tissues (Ratio of mean expression (RME) = 0.15, SE = 0.99, P value = 0.01). Expression of STAT3 was lower in total periodontitis tissues compared with total control tissues (RME = 0.20, SE = 0.95, P value = 0.02). Expression of STAT6 was higher in total periodontitis tissues compared with total control tissues (RME = 0.5.38, SE = 0.74, P value < 0.001). Expressions of other STAT genes were statistically similar in tissues obtained from cases and controls. Moreover, blood levels of all STAT genes were statistically similar between patients and controls. Correlation analysis demonstrated significant correlations between tissues levels of individual STAT genes as well as between their blood levels. However, tissue and blood levels of each STAT gene were not correlated. The current investigation potentiates the role of certain STAT genes in the development of this immune-related condition and warrants functional assays to clarify the mechanism.

Apoptotic Genes of Bax, Bad, Bcl2, and P53 in A549 Lung Cancer Cells Comparison of the Effect of Echinophora platyloba DC. Extract and Cordia myxa L Extract on the Expression of Apoptotic Genes of Bax, Bad, Bcl2, and P53 in A549 Lung Cancer Cells.

INTRODUCTION: Lung cancer is the most deadly and sumptuous cancer across the globe. Cancer occurrence is increasing progressively and there is no ideal cure yet. Therefore, new therapeutic areas are needed. The use of herbal extracts due to its properties such as antioxidant activity, anti-proliferative effect, and few side effects can be promising in the treatment of cancer. This study aimed to compare the effect of Echinophora platyloba DC. and Cordia myxa L extracts on apoptosis induction in A549 cancer cells. MATERIALS AND METHODS: In this experiment, the A549 cell line was first cultured in DMEM medium containing 10% FBS and then treated with different concentrations of both compounds. MTT assay was performed to determine IC50 and to compare the viability of cells treated with different concentrations of Echinophora platyloba DC. and Cordia myxa L seed on days 1, 3 and 5. QRT-PCR test was used to investigate the effects of Echinophora platyloba DC. and Cordia myxa L with IC50 on apoptosis induction. RESULTS: MTT results showed that both plant extracts resulted in cell death and decreased viability of lung cancer cells. But the percentage of viability decreased by Echinophora platyloba DC. was more. Also, Echinophora platyloba DC. significantly increased the expression of Bax, P53 and Bad apoptotic genes and decreased the expression of Bcl2 gene, which induces apoptotic death and the cytotoxic effect of Echinophora platyloba DC. over Cordia myxa L. CONCLUSION: In comparing the effects of these two extracts Echinophora platyloba DC. was more effective than Cordia myxa L and had greater cytotoxicity on A549 cancerous cells in a lesser concentration and could be an appropriate drug candidate for the treatment of lung cancer.