Theranostic nanoparticles with multifunctional ability have been emerging as a new platform for biomedical applications such as imaging, sensing and drug delivery. Despite gold nanorods (Au NRs) being an excellent nanosource with multifunctional versatility, they have certain limitations in biomedical applications, which include surfactant toxicity, biological stability and controlled drug release kinetics. Herein, we have developed Au NR-doxorubicin conjugates (DOX@PSS-Au NR) with improved drug loading efficiency (55 AE 6%) and minimum CTAB toxicity, by employing Au NRs (4.4 AE 0.5 aspect ratio) coated with poly(sodium 4-styrenesulfonate) (PSS). DOX@PSS-Au NR conjugates exhibited higher biological stability with sustained drug release kinetics at pH 5. The binding events of DOX molecules onto the PSS coated gold nanorods (PSS-Au NRs) were monitored through fluorescence quenching and the longitudinal surface plasmon resonance signals. Furthermore the anti-cancer potential and apoptosis inducing efficiency of DOX@PSS-Au NR conjugates in MCF-7 cells revealed higher therapeutic efficiency than free DOX, as corroborated through morphological assessment and in vitro cytotoxicity assay. In addition, DOX@PSS-Au NR conjugates showed efficient cellular entry and uniform intracellular distribution, suggesting the augmenting effect of chemotherapeutic drugs by Au NRs. Thus DOX@PSS-Au NR conjugates demonstrate significant therapeutic potential, suggesting their potential in anticancer therapy.

Herein, we report facile theranostic platinum nanoparticles (PtNPs) conjugated to an anticancer drug, doxorubicin (DOX), in unraveling the inhibition of a cell survival PI3K/AKT (phosphatidylinositol 3-kinase/protein kinase B) signaling pathway in MCF-7 and MDA-MB-231 human breast cancer cells. The significant features of our DOX@PtNPs as a theranostic platform are as follows: (i) drug release studies showed a progressive pH-dependent delivery; (ii) in vitro studies of DOX@PtNPs displayed a relatively higher cytotoxicity to breast cancer cells compared to unconjugated PtNPs and DOX; (iii) intracellular drug release studies showed a specific binding of DOX@PtNPs and their release within the cytoplasm and perinuclear region; (iv) DOX@PtNPs induced the apoptosis of cancer cells by DNA damage via the generation of elevated levels of reactive oxygen species and decreased mitochondrial membrane potential (ΔΨm), as evidenced by fluorescence microscopic studies; and (v) DOX@PtNPs inhibited the PI3K/AKT signaling pathway in breast cancer cells by activating PTEN, a tumor suppressor gene. The induced mitochondrial-dependent apoptotic pathway led to the activation of downstream caspases. Finally, our findings illustrate that DOX@PtNPs may serve as a better theranostic agent for cancer nanomedicine.

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In recent years, the development of a nano-conjugate system for drug delivery applications has gained attention among researchers.