Breast cancer is the most leading cancer and high mortality among women in worldwide [[1], [2], [3]]. Breast cancer has distinct subtypes which are broadly classified into four groups based on the presence of estrogen receptor (ER), progesterone (PR) and human epidermal growth factor receptor (HER2) [4,5] and they are Luminal A, Luminal B, HER-positive, and Triple-negative breast cancer (TNBC) [6]. TNBC is highly invasive and aggressive because it lacks all three above-mentioned receptors [7]. Consequently, there is always a need to find a way to treat TNBC type of breast cancer. Breast cancer treatment may consist of chemotherapy, radiation, hormone therapy, and surgery [8]. As there is absence of ER, PR, and HER2 [ 9], there is no scope for hormonal therapy in TNBC [[10], [11], [12]]. Therefore, chemotherapy has been the primary treatment for TNBC [13]. Currently, metal-based chemotherapeutic compounds are available as potent anti-cancer medications that can be used to treat breast cancer [[14], [15], [16]]. For example, copper based chemotherapeutic drug, phenanthroline copper(II) complex inhibited cell growth and induced cell death in TNBC cells [17]. Platinum based drug, cisplatin and carboplatin inhibited the cell cycle progression and metastasis of TNBC cells [18,19]. Although the platinum-based drugs are widely used, and are limited. This is because of acquired or inherent resistance by the cancer cells, non-specific toxicity and their inability to stop cancer reoccurrence [[20], [21], [22]]. These drawbacks have diverted the scientific community towards the development of non‑platinum metal-based pharmaceuticals [23]. Ruthenium complexes are a class of non‑platinum metal complexes which are the promising alternatives to platinum-based chemotherapeutic agents due to their unique biochemical properties [[24], [25], [26], [27]]. Ruthenium complexes exhibited superior anticancer activity on various types of cancer, which are overcoming the activity of cisplatin [28,29]. Ruthenium complexes inhibited the proliferation, cell adhesion and migration of TNBC cells were reported their inhibition on cell growth, metastasis and apoptosis by inducing cell cycle arrest in lung cancer cells [ 30,31]. In addition, the apoptotic cell death induced by ruthenium complexes by regulating PI3K/Akt signaling pathway in breast cancer cells were also performed [[32], [33], [34]].

An established genetic model organism, Caenorhabditis elegans, a eukaryotic multicellular organism with a fully sequenced genetic profile, is useful for studying aging [35,36]. In recent decades, C. elegans has served as a valuable in vivo model system to study both metabolic and genomic abnormalities to understand most human diseases [37]. In fact, gerontogenes and signaling pathways play a role in stress, longevity, and protein homeostasis in C. elegans [38]. In addition, we reported previously that organoruthenium(II) complexes enhanced the expression of downstream effector target SOD-3 in C. elegans and promote the nuclear accumulation of DAF-16 [39]. The tumoral C. elegans strain JK1466 (gld-1(q485)), which bears a mutation in the gld-1 tumor suppressor gene. In gld-1(q485) mutants, germ cells undergo a failure to exit from mitosis, persistently proliferating throughout the gonad; thus leads to the development of a lethal germline tumor in the animal.gld-1 encodes an ortholog of human QKI (KH domain containing RNA binding) [40]. Loss of function of gld-1 induced the ectopic trans differentiation of germ cells into various somatic cell types, giving rise to human germ cell tumor-like teratomas [41]. The sizes of the gonads were assessed from the loop region to the proximal region, encompassing the uterus area when occupied by tumorous cells. Gonad tumor morphology was characterized and visualized using DAPI and Acridine Orange staining. Herein, we have determined the effect of our complexes on tumor gonad reduction and its influence on the lifespan of JK1466 worms prior to the in vitro studies.