## 4 Concluding Remarks  
The involvement of molecular chaperones, including Hsp60, in carcinogenesis has been suggested by various findings [161; 107; 162]. Molecular chaperones have been found increased in tumor tissues and closely associated with tumor growth and aggressiveness. Along the same lines, decreased levels and expression of chaperones have been found associated with reduced cancer cell proliferation, motility, survival, and metastasization, and with decreased neoangiogenesis and resistance to anti-tumor immune response and treatment [163; 164; 165; 166; 167]. The quantitative variations of Hsp60 during carcinogenesis, especially its increase, may be simply the reflection of increased metabolic and proliferative activities of the cancer cell, which would require more chaperonin molecules than a normal cell at its physiological level of metabolism and proliferation. Nevertheless, the role of Hsp60 can still be considered pro-tumoral even if it is not a distinct carcinogenic factor. It would be an example of chaperonopathy by mistake or collaborationism, meaning that the human molecule helps the tumor to grow, proliferate, metastasize, and resist stressors such as anti-cancer drugs. It is crucial to visualize this situation because it then appears very clearly that therapeutic strategies aiming at inhibiting-blocking the chaperonin (negative chaperonotherapy) in tumor cells may offer efficacious ways to defeat cancer. Therefore, \begin{table}
\begin{tabular}{c c c c} \hline \hline
**Tissue** & \begin{tabular}{c} **miRNAs and** \\ **miRNAs Status** \\ \end{tabular} & **Effect** & **Reference** \\ \hline Rat cardiomyocytesocytes & \begin{tabular}{c} miR-1 and miR-206 \\ high-glucose-dependent \\ up-regulation \\ \end{tabular} & \begin{tabular}{c} Increased cell apoptosis induced \\ by Hsp60 and IGF-1 \\ down-regulation and IGF-1/IGF-1R/PI3 K/Akt \\ pathway inhibition \\ \end{tabular} & [158; 159] \\ \hline Breast cancer & \begin{tabular}{c} miR-29a in vitro \\ down-regulation \\ \end{tabular} & \begin{tabular}{c} Increased cancer cell apoptosis \\ and sensitization to anti-cancer \\ treatment induced by Hsp60 \\ up-regulation \\ \end{tabular} & [155] \\ \hline Gastric Lymphoma & miR-17 higher level & \
\begin{tabular}{c} Increased malignancy via \\ regulation of Hsp60/TNF2 \\ pathway \\ \end{tabular} & [160] \\ \hline Hepatocellular carcinoma & miR-644a in vitro &
\begin{tabular}{c} Increased cancer-cell apoptosis \\ induced by Hsp60 inhibition \\ \end{tabular} & [156] \\ \hline \hline \end{tabular}
\end{table} 
Table 3: Examples of miRNAs involved in Hsp60 regulation. negative chaperopathy, aiming to inhibit or block pro-tumorigenic molecular chaperones deserves investigation [63; 168; 169]. The role of Hsp60 in carcinogenesis is not yet fully understood, and its elucidation is complicated because it seems to vary depending on the tumor type, tissue affected, stage, and other unidentified factors. While some reports indicate that Hsp60 displays a protumor role others show the contrary [85; 90; 98; 117; 118; 119; 122]. While the exact role of Hsp60 in every tumor in which its levels and location changes is being studied, the quantitative variations and tissue distribution of the chaperin may be used as biomarkers potentially useful for diagnosis, prognostication, and disease monitoring [120; 123; 170; 171]. Additionally, investigations on Hsp60 chaperotherapy in its various forms should be performed and aiming at standardizing the use the chaperonin as a therapeutic target or agent [63].