Springer Science and Business Media LLC

Mitochondrial dysfunction is known to contribute to cancer initiation, progression, and chemo-and radio-resistance. However, the precise role of mitochondria in cancer is controversial. Hence, here we tried to further clarify the role of mitochondria in cancer by transferring healthy mitochondria to cancer cells, and also to cells with depleted mitochondrial DNA (ρ0). Healthy mitochondria were isolated from WI-38 cells and were transferred to HeLa, SAS, HeLa ρ0, and SAS ρ0 cells. Then, cell proliferation was verified. In addition, the cells were treated by different concentrations of cisplatin and assessed for apoptosis induction and quantifying the mRNA expression of apoptosis-related genes. Results revealed that incubation of the HeLa, SAS and HeLa ρ0 cells with 5 µg/ml of the isolated mitochondria for 24 h significantly (p < 0.001) increased cell proliferation compared to non-treated controls. Interestingly, the mitochondria transfer rescued the ρ0 cells and made them capable of growing under conventional culture medium. However, the number of apoptotic cells was significantly higher in the HeLa ρ0 cells that received the mitochondria (HeLa-Fibro-Mit) compared to the HeLa ρ0. Furthermore, the expression level of BCL-2 anti-apoptotic gene was down-regulated in both HeLa-Fibro-Mit and SAS-Fibro-Mit cell lines while the expression levels of the BAX, caspase8, caspase9, and AIF pro-apoptotic genes were upregulated. Our findings indicated that although the response of cancer cells to the mitochondria transfer is cancer-type dependent, but the introduction of normal exogenous mitochondria to some cancer cells might be considered as a potential novel therapeutic strategy.

Chickpea, commonly called Bengal gram or Garbanzo bean, faces a productivity crisis around the globe due to numerous biotic and abiotic stresses. The eroded genetic base of the cultivated Cicer gene pool is becoming a significant bottleneck in developing stress-resilient chickpea cultivars. In this scenario, the crop wild relatives (CWR) of chickpea, with the useful genomic wealth of their wild adaptation, give a ray of hope to improve the genetic background of the cultivated Cicer gene pool. To extrapolate these unearthed genomic diversities of wild, we require a thorough understanding of the pre-historic domestication episodes that are changing their shape with the expansion of the available scientific evidence. Keeping aforesaid in view, the current review article provides a glimpsed overview on several efforts done so far to reveal the mysterious origin and evolution of the Cicer gene pool, along with the constraints in their utilization for chickpea crop improvement. It encapsulates various stress-resilient CWR of chickpea and their use in several pre-breeding programs to develop numerous breeding populations for crop genetic enhancement. Further, this review will recapitulate the significant contributions of structural, functional and comparative genomics, pan-genomics and diverse genomics-assisted breeding strategy in dissecting the untapped trait-specific allelic/gene diversity and domestication pattern behind the CWR of chickpea, along with their potential and promises. We expect the newly explored genetic variations may be used in the breeding programs for re-wilding the cultigens’ genomic background to open a new avenue for genetic gain and crop improvement capacity of chickpea.

Paraquat (PQ) is a widely used and highly toxic pesticide that is often actively ingested and causes pulmonary fibrosis in patients. Ferroptosis is a regulated form of non-apoptotic cell death associated with iron-dependent lipid peroxidation. Previous studies have shown that ferroptosis is involved in the occurrence and development of acute lung injury (ALI). In this study, a model rat with inflammatory response, oxidative stress, lipid peroxidation, and pulmonary fibrosis was successfully established by PQ administration. The occurrence of ferroptosis in PQ model rats was confirmed by TUNEL staining, iron ion detection, and Ferroptosis related biomarkers detection. Western blotting (WB) and real-time PCR (RT-PCR) showed that the expression of Keap1 was significantly up-regulated and the expression of Nrf2 was significantly down-regulated in the lung tissue of PQ rats. Further transcriptomics and proteomics confirmed: (1) Enrichment of molecular processes related to iron ion binding; (2) Keap1 may promote Nrf2 ubiquitination and lead to Nrf2 degradation; (3) There is functional enrichment in ferroptosis related pathways. Our results suggest that PQ can regulate Keap1/Nrf2 signaling pathway, leading to increased lipid peroxidation and abnormal iron uptake, thereby inducing iron death and exacerbating the progression of pulmonary fibrosis. Our study provides new insights into PQ-induced pulmonary fibrosis.

The regulation of reactive oxygen scavengers against biotic and abiotic conditions were investigated in the seedling of Panax ginseng C. A. Meyer. From the EST library we selected the antioxidant marker genes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione synthase (GS). The abiotic chilling, heat, osmotic, oxidative, and wounding stresses and biotic stresses with fungal pathogens were tested against 3-week-grown seedlings. The expression patterns of the genes were analyzed by means of real-time quantitative RT-PCR. The transcriptome result under abiotic stresses showed differential expression and elevated up-regulation of PgSOD, PgGPX, PgGS, and PgAPX, thus it may prove the generation of ROS in ginseng. Whereas, in biotic stress the up-regulation of transcript level merely based on the incompatible interactions. But PgAPX and PgCAT showed no significant change or slight down-regulation of transcript level during pathogen interaction. Thus it may suggest that in ginseng, plant-pathogen interaction triggers defense-related gene transcription via salicylic acid mediated signaling mechanism, and also possess crosstalk signaling networks between abiotic and biotic stress responses.

Etiological factors for coronary artery disease (CAD) involve a wide range of gene and environmental interactions. One of the systems being implicated in the pathophysiology of CAD is the renin-angiotensin system (RAS). However, the genetic polymorphisms of this system have not been widely studied in Iranian patients diagnosed with CAD. The aim of this study was to assess the relationship between six gene polymorphisms of RAS components and CAD in a sample of Iranian population. A total of 374 participants were enrolled in a case/control study. The presence of CAD was determined by coronary angiography. Genotyping of six RAS gene polymorphisms was performed using a modified PCR–RFLP method. Our results revealed, for the first time, a significant independent association of angiotensin-converting enzyme (ACE) A-240T polymorphism and incidence of CAD among Iranian women (P = 0.005, OR = 20.4, 95 % CI = 2.49–41.2). There has also been a significant difference in genotype distribution of ACE A-240T (P = 0.008) and angiotensin II receptor type 2 C3123A polymorphism (P = 0.032) in Iranian female participants. In conclusion, TT genotype of ACE A-240T seems to be a genetic risk factor for CAD in Iranian women.

The role of serum-based biomarkers such as microRNAs in cancer diagnosis has been extensively established. This study aimed to determine the expression levels of bioinformatically selected miRNAs and whether they can be used as biomarkers or a new therapeutic target in patients with acute lymphoblastic leukemia (ALL). The expression levels of serum miR-22, miR-122, miR-217, and miR-367 in 21 ALL patients and 21 healthy controls were measured using quantitative real-time PCR. The receiver operating characteristic (ROC) curve and the associated area under the curve (AUC) was used to assess candidate miRNAs’ diagnostic value as a biomarker. The results showed that miR-217 was markedly decreased in patients with ALL compared to controls. Moreover, miR-22, miR-122, and miR-367 were found to be upregulated. Furthermore, ROC analysis showed that serum miR-217 and miR-367 could differentiate ALL patients from healthy individuals, while miR-22 has approximate discriminatory power that requires further investigation. These results provide promising preliminary evidence that circulating miR-217 and miR-367 could be considered potent diagnostic biomarkers and therapeutic goals in this disease.