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Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...

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Silymarin-Loaded, Lactobionic Acid-Conjugated Porous PLGA Nanoparticles Induce Apoptosis in Liver Cancer Cells.

Priyanka Upadhyay¹, Mousumi Bhattacharjee¹, Saurav Bhattacharya¹

¹Centre for Research in Nanoscience and Nanotechnology, Technology Campus, University of Calcutta, JD2, Sector III, Salt Lake City, Kolkata 700106, India.

ACS Applied Bio Materials

|January 12, 2022

Summary

Lactobionic acid-adorned nanoformulations of silymarin (LA-PLGA-Sil) show enhanced anticancer effects against HepG2 cells by targeting the miR-29b/p53 axis. This novel approach activates apoptosis and inhibits proliferation, offering a promising strategy for hepatocellular carcinoma (HCC) treatment.

Keywords:

HCC NFκB-p65 lactobionic acid miR-29b nanoformulations p53 silymarin

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Area of Science:

Biomedical Engineering
Nanotechnology
Cancer Biology

Background:

Hepatocellular carcinoma (HCC) cells like HepG2 require effective and targeted treatments.
Silymarin, a natural flavonoid, exhibits anticancer properties.
Nanoencapsulation can improve drug delivery and efficacy.

Purpose of the Study:

To compare the efficacy of lactobionic acid-adorned porous PLGA-encapsulated silymarin (LA-PLGA-Sil) with plain porous PLGA-encapsulated silymarin (PLGA-Sil) against HepG2 cells.
To elucidate the molecular mechanisms underlying the anticancer activity of LA-PLGA-Sil.

Main Methods:

Synthesis and characterization of LA-PLGA-Sil and PLGA-Sil nanoformulations.
In vitro treatment of HepG2 cells with nanoformulations.
Assessment of cell viability, apoptosis, cell-cycle arrest, and microRNA expression.
Analysis of key protein expressions including p53 and NFκB-p65.

Main Results:

LA-PLGA-Sil demonstrated significantly higher cytotoxicity against HepG2 cells at lower doses compared to PLGA-Sil, attributed to enhanced targeting by lactobionic acid.
LA-PLGA-Sil treatment induced apoptosis and cell-cycle arrest in HepG2 cells via activation of the p53 pathway and stabilization of NFκB-p65.
LA-PLGA-Sil upregulated miR-29b, which targeted Bcl-2, leading to apoptosis, and also impaired HepG2 cell migratory activity.

Conclusions:

LA-PLGA-Sil is a potent nanoformulation for HCC treatment, exhibiting superior efficacy over PLGA-Sil.
The anticancer mechanism involves targeting the miR-29b/p53 axis and stabilizing NFκB, promoting apoptosis and inhibiting migration.
This study highlights the therapeutic potential of LA-PLGA-Sil for hepatocellular carcinoma.